Development Of Cardiovascular Disease Research Articles

A Body Shape Index as a Simple Anthropometric Marker for the Risk of Cardiovascular Events.

To provide an overview of the predictive value of A Body Shape Index (ABSI) for the risk of cardiovascular events. ABSI has been reported to have an association with development of cardiovascular diseases, and its usefulness for predicting major cardiovascular events including cardiovascular mortality, nonfatal coronary syndrome and nonfatal stroke has been investigated. The formula for ABSI includes waist circumference, which is not included in the conventional calculation of body mass index (BMI), along with BMI and height. High ABSI is independently associated with a high incidence of cardiovascular events. ABSI with specific cutoff values can be a useful tool for cardiovascular risk stratification by detecting the presence of abdominal obesity and it can be used for evaluation of the risk of cardiovascular events. Nonetheless, other factors such as race, gender, age, and physical, environmental and socioeconomic purviews also need be taken into consideration.

Fatty acid binding protein 3 activates endothelial adhesion of circulating monocytes and impairs endothelial angiogenesis.

Vascular inflammation and endothelial dysfunction cause the development of atherosclerotic cardiovascular diseases including coronary artery disease (CAD). While elevated fatty acid binding protein 3 (FABP3) may be associated with the presence of cardiovascular diseases, its mechanistic effects remain unclear. This study aimed to investigate the role of FABP3 in impaired angiogenesis and the development of atherosclerosis in CAD. In total, 1104 patients were enrolled in a clinical observational study and the correlation between serum FABP3 and cardiovascular events were analysed. Another group of CAD patients and non-CAD subjects were enrolled, and their plasma FABP3 concentrations were measured. Primary cultured mononuclear cells endothelial progenitor cells and human coronary artery endothelial cells were used in vitro. Matrigel plug neovascularisation assay and the aortic ring assay were used in wild-type and apolipoprotein E-knockout mice in vivo. Circulating FABP3 was up-regulated in the cardiovascular event-positive group and in the CAD patients. Mononuclear cells from the CAD patients presented increased expression of FABP3. FABP3 enhanced the expression of adhesion molecules, including integrin β2, integrin α4 and PSGL1 in mononuclear cells. FABP3 caused endothelial cell dysfunction through the ERK/p38/STAT1/VEGF signalling pathway. Moreover, oxLDL or TNF-α stimulations impaired endothelial cell function through FABP3-dependent signalling pathways. FABP3 also impaired in vivo angiogenesis. This study elucidates the clinical and pathological impact of FABP3 on atherosclerotic CAD. Future research may be necessary to evaluate whether FABP3 could be a therapeutic target, especially with regard to stable CAD.

A novel approach to the prevention and management of chemotherapy-induced cardiotoxicity: PANoptosis.

As a fundamental component of antitumor therapy, chemotherapy-induced cardiotoxicity (CIC) has emerged as a leading cause of long-term mortality in patients with malignant tumors. Unfortunately, there are currently no effective therapeutic preventive or treatment strategies, and the underlying pathophysiological mechanisms of CIC remain inadequately understood. A growing number of studies have shown that different mechanisms of cell death, such as apoptosis, pyroptosis, and necroptosis, are essential for facilitating the cardiotoxic effects of chemotherapy. The PANoptosis mode represents a highly synchronized and dynamically balanced programmed cell death (PCD) process that integrates the principal molecular characteristics of necroptosis, apoptosis, and pyroptosis. Recent research has revealed a significant correlation between PANoptosis and the apoptosis of tumor cells. Chemotherapy drugs can activate PANoptosis, which is involved in the development of cardiovascular diseases. These findings suggest that PANoptosis marks the point where the effectiveness of chemotherapy against tumors overlaps with the onset and development of cardiovascular diseases. Furthermore, previous studies have demonstrated that CIC can simultaneously induce pyrodeath, apoptosis, and necrotic apoptosis. Therefore, PANoptosis may represent a potential mechanism and target for the prevention of CIC. This study explored the interactions among the three main mechanisms of PCD, pyroptosis, apoptosis, and necroptosis in CICs and analyzed the relevant literature on PANoptosis and CICs. The purpose of this work is to serve as a reference for future investigations on the role of PANoptosis in the development and mitigation of cardiotoxicity associated with chemotherapy.

Roles of SIRT3 in cardiovascular and neurodegenerative diseases.

Sirtuin-3 (SIRT3) in mitochondria has nicotinamide adenine dinucleotide (NAD+)-dependent protein deacetylase activity. As such, SIRT3 is crucial in cardiovascular and neurodegenerative diseases. Advanced proteomics and transcriptomics studies have revealed that SIRT3 expression becomes altered when the heart or brain is affected by external stimuli or disease, such as diabetic cardiomyopathy, atherosclerosis, myocardial infarction, Alzheimer's disease, Huntington's disease, and Parkinson's disease. More specifically, SIRT3 participates in the development of these disorders through its deacetylase activity and in combination with downstream signaling pathways. The paper reviews SIRT3's expression changes, roles, and mechanisms associated with the development of cardiovascular and neurodegenerative diseases. Additionally, strategies targeting SIRT3 to treat or regulate cardiovascular and neurodegenerative disease development are discussed.

Hydrogen sulfide attenuates disturbed flow-induced vascular remodeling by inhibiting LDHB-mediated autophagic flux

Disturbed flow (DF) plays a critical role in the development and progression of cardiovascular disease (CVD). Hydrogen sulfide (H2S) is involved in physiological processes within the cardiovascular system. However, its specific contribution to DF-induced vascular remodeling remains unclear. Here, we showed that the H2S donor, NaHS suppressed DF-induced vascular remodeling in mice. Further experiments demonstrated that NaHS inhibited the proliferation and migration of vascular smooth muscle cells (VSMCs) induced by platelet-derived growth factor-BB (PDGF), as well as the autophagy triggered by DF and PDGF. Mechanistically, RNA-Seq results revealed that NaHS counteracted the PDGF-induced upregulation of lactate dehydrogenase B (LDHB). Overexpression of LDHB abolished the protective effect of NaHS on DF-induced vascular remodeling. Furthermore, LDHB interacted with vacuolar-type proton ATPase catalytic subunit A (ATP6V1A), leading to lysosomal acidification, a process that was attenuated by NaHS treatment. The residues of leucine (Leu) 57 in ATP6V1A and serine (Ser) 269 in LDHB are critical for their interaction. Notably, the expression of LDHB was found to be elevated in vascular tissues from patients with abdominal aortic aneurysms (AAA) and thoracic aortic aneurysms (TAA). These data identify a molecular mechanism by which H2S attenuates DF-induced vascular remodeling by inhibiting LDHB and disrupting the interaction between LDHB and ATP6V1A, thereby impeding the autophagy process. Our findings provide insight that H2S or targeting LDHB has therapeutic potential for preventing and treating vascular remodeling.

Unlocking the Potential of miRNAs in Sepsis Diagnosis and Prognosis: From Pathophysiology to Precision Medicine.

The clinical syndrome appears as a dysregulated host response to infection that results in life-threatening organ dysfunction known as Sepsis. Sepsis is a serious public health concern where for every five deaths in ICU there is one patient who dies with sepsis worldwide. Sepsis is featured as unbalanced inflammation and immunosuppression which is sustained and profound, increasing patient susceptibility to secondary infections and mortality. microRNAs (miRNAs) play a central role in the control of many biological processes, and the deregulation of their expression has been linked to the development of oncological, cardiovascular, neurodegenerative, and metabolic diseases. In this review, we discuss the role of miRNAs in sepsis pathophysiology. Overall, miRNAs are seen as promising biomarkers, and it has been proposed to develop miRNA-based diagnosis and therapies for sepsis. Yet, the picture is not so straightforward because of miRNAs' versatile and dynamic features. More research is needed to clarify the expression and role of miRNAs in sepsis and promote the use of miRNAs for sepsis management. This study provides an extensive, current, and thorough analysis of the involvement of miRNAs in sepsis. Its purpose is to encourage future research in this area, as tiny miRNAs have the potential to be used for rapid diagnosis, prognosis, and treatment of sepsis.

Development and implementation of a digiphysical screening model with nationwide reach to diagnose familial hypercholesterolemia.

Familial hypercholesterolemia (FH) is a hereditary dyslipidemia that confers a severely elevated risk for development of early atherosclerotic cardiovascular disease if left untreated. FH is underdiagnosed in most countries including Sweden. To develop and evaluate the implementation of a digiphysical screening model to diagnose FH in the clinical routine. A digiphysical screening model for FH, containing digital and physical related activities was developed and fully implemented in routine clinical care in the Stockholm region, Sweden 2022. The centerpiece of the model is a tailormade interactive web-based platform designed to facilitate communication and secure medical information exchange between its participants and the healthcare professionals. The screening model includes, (i) cascade screening of relatives to patients with a confirmed FH diagnosis and (ii) systematic selective screening of patients with established atherosclerotic coronary artery disease. Until October 2023, 338 index patients were included in the cascade screening. They invited 954 relatives nationwide, 616 (64.6%) accepted participation, 346 (36.3%) were completely screened, and 141 (14.8%) have received a FH diagnosis (40.8% of all completely screened). Selective screening was performed in 2867 patients with coronary artery disease, 355 (12.4%) were identified with increased risk for FH and underwent a genetic test. Of these, 153 (3.8%) had a genetic test result and 52 (1.8%) were diagnosed with FH. A digiphysical screening model with a nationwide reach to diagnose FH was successfully implemented in routine clinical care. The model has potential to facilitate FH screening and provide health economic benefits long term.

Prevalence and Mortality Trends of Hypertension Subtypes Among US Adults: An Analysis of the National Health and Nutrition Examination Survey (NHANES).

Hypertension (HTN) has been demonstrated as one of the leading risk factors for development of cardiovascular disease (CVD) and CVD mortality. This study examines the prevalence and distribution of HTN subtypes (isolated diastolic hypertension [IDH], isolated systolic hypertension [ISH], and systolic-diastolic hypertension [SDH]) across age, sex, and race/ethnicity per the nationally representative National Health and Nutrition Examination Survey (NHANES) from 1999 to 2020 based on the updated 2017 ACC/AHA HTN definition. We further examined for associations of each subtype with CVD and all-cause mortality using Cox regression analysis. Among US adults, the overall prevalence of HTN is 47.4%. Across increasing age, the prevalence of IDH decreased, ISH increased, and SDH increased and peaked in the 6th decade of life after which SDH prevalence decreased. By age 80, over 80% of persons with HTN demonstrated ISH. A sub-cohort from NHANES 1999-2008 with follow-up until 2018 showed that ISH and SDH were most strongly associated with increased risk for CVD (HR 1.18, 95% CI 1.01-1.38; HR 1.31, 95% CI 1.07-1.60, respectively) and all-cause mortality (HR 1.17, 95% CI 1.06-1.28; HR 1.21, 95% CI 1.08-1.37, respectively). Our data demonstrate the continuing importance of HTN subtype transitions across age and their differences in predicting future CVD and total mortality.

150 Pediatric to adolesence populations‘ oral health and it's biomarkers as indicators for development of cardiovascular disease: a systematic review

150 Pediatric to adolesence populations‘ oral health and it's biomarkers as indicators for development of cardiovascular disease: a systematic review

Immunomodulation for accelerated atherosclerosis in rheumatoid arthritis and systemic lupus erythematosus.

In the last decades, consisting evidence supported a close relationship between both innate and adaptive immune systems and the accelerated cardiovascular (CV) disease characterizing autoimmune diseases, such as systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA). Indeed, several cell lines involved in the pathogenesis of these autoimmune diseases, such as macrophages and dendritic cells, as well as different T and B lymphocyte subsets, and inflammatory cytokines, have been demonstrated to be directly involved in the mechanisms underlying early atherosclerotic arterial wall damage. Traditional CV risk factors play a concomitant role but do not sufficiently account for the increased prevalence of CV disease in these patients. Indeed, the pathophysiological link between RA and SLE and atherosclerosis is based on complex inflammatory pathways that interconnect these conditions and may explain the significant morbidity and mortality rates demonstrated in these patients, with consequent significant negative effects on quality of life and long-term survival. Consequently, it is intriguing to hypothesize that immunosuppressive drugs commonly used in the treatment of these pathologies may also exert an immunomodulatory and anti-inflammatory effect in mitigating the atherosclerotic damage that has been demonstrated to occur early in the initial stages of the disease. Recognizing risk factors, predicting occurrences and early intervention to prevent CV disease development have emerged as critical objectives in RA and SLE treatment. In this review, we aimed to provide an updated overview of the atherogenic effects exerted by the immune and inflammatory pathways involved in the pathogenesis of RA and SLE. Moreover, we examined the available evidence which may support the potential effects of immunosuppressive therapies in reducing CV damage and, consequently, CV disease risk in these patients.

The association between systemic inflammation markers and the risk of incident dilated cardiomyopathy: a prospective study of 351,148 participants

Background The role of systemic inflammation in the development and progression of cardiovascular diseases has been attractive, but its association with incident dilated cardiomyopathy (DCM) is rarely investigated. This study aimed to systematically investigate the association between various inflammatory markers and DCM incidence. Methods The data were derived from the UK Biobank database. Systemic inflammation markers in this study encompassed peripheral immune cell counts and their ratios and the low-grade inflammation score (INFLA-score). The Cox proportional hazards regression, restricted cubic splines model, and segmented regression were adopted to assess the association between systemic inflammation markers and DCM incidence. Additionally, the subgroup Cox analysis stratified across sex was also performed. Results A total of 351,148 participants were enrolled in this study, and 377 subjects developed DCM during a mean follow-up of 12.21 years. The positive association between C-reactive protein (CRP), neutrophil-to-lymphocyte ratio (NLR), and CRP-to-lymphocyte ratio (CLR) and DCM incident risk was found (CRP: HR = 1.190, P = 0.001; NLR: HR = 1.315, P = 0.033; CLR: HR = 1.206, P < 0.001), while the lymphocyte-to-monocyte ratio (LMR) was negatively associated with DCM incident risk (HR = 0.756; P = 0.033). Furthermore, the increased risk of DCM incidence was significantly and nonlinearly correlated with the reduction of platelet count (HR = 0.543; P = 0.002). In the subgroup analysis, sex-specific inflammation markers related to DCM development were noticed. Conclusions The study has underlined that multiple inflammation markers were significantly associated with the risk of incident DCM, which would provide evidence for the aetiological study of DCM.

The Impact of Glomerular Disease on Dyslipidemia in Pediatric Patients Treated with Dialysis

Background/Objectives: Children on dialysis have a 10-fold increase in cardiovascular disease (CVD)-related mortality when compared to the general population. The development of CVD in dialysis patients is attributed to Chronic Kidney Disease–Mineral Bone Disorder (CKD-MBD) and dyslipidemia. While the prevalence of dyslipidemia in adult dialysis patients has been described, there are limited data on prevalence, severity, and risk factors for pediatric dyslipidemia. Methods: Data from 1730 pediatric patients ≤ 21 years receiving maintenance hemodialysis or peritoneal dialysis with at least one lipid panel measurement were obtained from USRDS between 2001 and 2016. Disease etiology was classified as being glomerular (n = 1029) or non-glomerular (n = 701). Comparisons were made across etiologies using both linear and logistic regression models to determine the relationship between disease etiology and lipid levels. Results: The cohort had a mean age of 15.2 years and were 54.5% female. Adjusting for age, sex, race/ethnicity, modality, time with End Stage Kidney Disease (ESKD), and body mass index (BMI) and using non-glomerular etiology as the reference, glomerular disease [mean (95% CI)] was associated with +19% (+14.7%, +23.8%) higher total cholesterol level (183 mg/dL vs. 162 mg/dL), +21% (+14.8%, +26.6%) higher low density lipoprotein cholesterol level (108 mg/dL vs. 87 mg/dL), and +22.3% (+15.5%, +29.5%) higher triglyceride level (169 mg/dL vs. 147 mg/dL). Glomerular disease [OR (95% CI)] was associated with 3.0-fold [2.4, 3.9] higher odds of having an abnormal total cholesterol level, 3.8-fold [2.8, 5.0] higher odds of having an abnormal LDL-C level, and 1.9-fold [1.5, 2.4] higher odds of having an abnormal triglyceride level when compared to non-glomerular disease. Conclusions: Pediatric dialysis patients have a high prevalence of dyslipidemia, particularly from elevated triglyceride levels. Specifically, patients with glomerular disease have an even higher risk of dyslipidemia from elevated non-HDL cholesterol and triglyceride levels than patients with non-glomerular disease. The long-term impact of this unfavorable lipid profile requires further investigation.

The Impact of Dietary Fiber on Cardiovascular Diseases: A Scoping Review

Background/Objectives: Cardiovascular disease (CVD) remains a leading cause of morbidity and mortality globally, placing an ever-increasing burden on healthcare systems. Dietary factors play a crucial role in the development and progression of CVD. Among them, dietary fiber has emerged as a potential modifiable factor with the potential to impact CVD risk. However, the specific and independent effects of dietary fiber on CVD are still not fully understood, making this area of research both challenging and of great significance. Methods: The publications of human studies involving the impact of dietary fiber on CVD were retrieved from databases including PubMed, Embase, Web of Science, Scopus, Cochrane Library, CBM, and China National Knowledge Infrastructure (CNKI). A search was conducted within these databases for studies published between 2014 and 20 March 2024. The included literature was screened and summarized. Results: A total of seven articles were included, and the related studies encompassed various types of dietary fiber, including soluble and insoluble dietary fiber, as well as research from different countries and regions. The outcome indicators involved an important measure known as the hazard ratio (HR). Conclusions: Increasing the intake of dietary fiber could reduce the risk of cardiovascular diseases through various mechanisms. To increase the consumption of dietary fiber from multiple sources, it would be beneficial to develop and promote healthcare interventions to enhance people’s awareness of the health benefits of dietary fiber, promote the consumption of fiber-rich foods, and advocate for a healthier diet.

Gut Microbiota Alterations in Patients With Kawasaki Disease.

The intestinal microbiota influences many host biological processes, including metabolism, intestinal barrier functions, and immune responses in the gut and distant organs. Alterations in its composition have been associated with the development of inflammatory disorders and cardiovascular diseases, including Kawasaki disease (KD). KD is an acute pediatric vasculitis of unknown etiology and the leading cause of acquired heart disease in children in the United States. The presence of gastrointestinal symptoms in the acute phase of KD has been associated with an increased risk of treatment resistance and the development of coronary artery aneurysms. Studies report alterations in fecal bacterial communities of patients with KD, characterized by the blooming of pathogenic bacteria and decreased relative abundance of short-chain fatty acid-producing bacteria. However, causality and functionality cannot be established from these observational patient cohorts of KD. This highlights the need for more advanced and rigorous studies to establish causality and functionality in both experimental models of KD vasculitis and patient cohorts. Here, we review the evidence linking an altered gut microbiota composition to the development of KD, assess the potential mechanisms involved in this process, and discuss the potential therapeutic value of these observations.

Menopausal Hormone Therapy: Its Role in the Prevention of Cardiovascular Diseases and the Risk of Breast Cancer in Women

Objective: This review was conducted to explain how menopausal hormone therapy (MHT) benefits cardiovascular diseases (CVDs) and how to control the risk of breast cancer. Mechanism: Estrogen deficiency, altered energy homeostasis, adipocyte changes, inflammation, and insulin resistance are responsible for the development of metabolic syndrome and CVDs. Estrogen influences hypothalamic function and maintains the energy balance, protecting menopausal women from these cardiovascular risk factors. However, estrogen metabolism plays a crucial role in the genotoxic pathway that leads to breast cancer. Moreover, MHT is associated with cell proliferation and mutation signaling pathways in breast cancer, as well as the process of growing the breast cancer stem cell. Findings in Brief: While MHT may have favorable effects when started early, introducing it later in the course of atherosclerosis may pose major dangers, underlining the importance of timing in hormone therapy. Estrogen-only therapy has a greater favorable effect on CVDs than the estrogen-progesterone combination. Although the connection between MHT and breast cancer is well-documented, significant knowledge gaps remain, especially regarding the long-term effects of newer MHT formulations. Current studies support using the lowest effective dose for the shortest possible duration, with a focus on tailoring therapy to individual risk factors, such as obesity, smoking, and alcohol consumption. Thus, MHT should be customized due to the intricacy of individual risk factors and differences in responses to therapy. Conclusions: Although MHT is effective for controlling CVDs in women entering menopause, it must be used with caution, especially in women at high risk of breast cancer.

Mitochondrial quality control: Biochemical mechanism of cardiovascular disease.

Mitochondria play a key role in the regulation of energy homeostasis and ATP production in cardiac cells. Mitochondrial dysfunction can trigger several pathological events that contribute to the development and progression of cardiovascular diseases. These mechanisms include the induction of oxidative stress, dysregulation of intracellular calcium cycling, activation of the apoptotic pathway, and alteration of lipid metabolism. This review focuses on the role of mitochondria in intracellular signaling associated with cardiovascular diseases, emphasizing the contributions of reactive oxygen species production and mitochondrial dynamics. Indeed, mitochondrial dysfunction has been implicated in every aspect of cardiovascular disease and is currently being evaluated as a potential target for therapeutic interventions. To treat cardiovascular diseases and improve overall heart health, it is important to better understand these biochemical systems. These findings allow the achievement of targeted therapies and preventive measures. Therefore, this review investigates different studies that demonstrate how changes in mitochondrial dynamics like fusion, fission, and mitophagy contribute to the development or worsening of disorders related to heart diseases by summarizing current research on their role.

The Association between the Consumption of Dairy Products and the Risk of Cardiovascular Disease: Tehran Lipid and Glucose Study

Background and Objectives: The association between the consumption of dairy products and the risk of cardiovascular disease (CVD) is not well-known yet. Here, we aimed to determine the potential effects of total intake and subtypes of dairy products on the development of CVD in an Iranian adult population. Methods: Among adult participants of the third phase of the Tehran Lipid and Glucose Study (TLGS), after excluding those with incomplete dietary, biochemical and anthropometric data, and those who had CVD events at baseline, 2635 adults were selected and followed up till the sixth phase of the TLGS. Baseline dietary intakes were evaluated using a validated food frequency questionnaire with 168 items. There was no significant difference between the baseline characteristics of participants who did not complete the FFQ and those of the total population in the third phase of the TLGS. Finally, the risk of CVD events after adjusting for potential confounding variables was evaluated across the tertile categories of dairy products using the Cox proportional hazard regression models. Results: During a 10.6-year follow-up, the incidence rate of CVD was 6.5%. After adjusting for confounding factors, there was no significant association between CVD risk and total dairy, low-fat and high-fat dairy, fermented and non-fermented dairy products, high- and low-fat milk, high- and low-fat yogurt, cheese, and cream cheese, as well as ice cream. Conclusion: According to numerous evidence in previous studies that revealed there is no association between the consumption of dairy products, and CVD risk, independent of high-fat or low-fat dairy products. Hence, it is vital to reconsider dietary recommendations on lowering the intake of high-fat dairy products for the prevention of CVD.

Addressing cardiovascular health risk factors in American Indian/Alaska Native Children: A narrative review

Background Cardiovascular disease (CVD) is common in American Indian/Alaska Native (AI/AN) adults and represents the leading cause of mortality. Risk factors for CVD in AI/AN adults are well-described, and a growing body of evidence reports the inequitable prevalence of factors associated with the development of CVD in AI/AN children, including obesity, physical inactivity, and diabetes mellitus (DM). Objective This article organizes and summarizes the evidence describing CVD risk factors in AI/AN children, discusses the social drivers of health impacting these risks, and highlights several programs that have demonstrated effectiveness in improving AI/AN child health. Results Fortunately, multiple community- and Tribal-based programs have aimed to mitigate the impact of obesity, diabetes, and physical activity in AI/AN youth, given that nascent CVD begins in the pediatric years. These efforts include screening, lifestyle choices, including diet and exercise, and, importantly, culturally relevant programming to promote cardiovascular health in AI/AN children. Discussion Though at a disproportionate risk for CVD based on biological and social drivers of health, AI/AN children are being prioritized by their communities, and there are many ongoing efforts to support their cardiovascular health. However, further investigation and investment is warranted to protect this population and address ongoing disparities in AI/AN CVD.

Effects of changes in body composition on cardiometabolic diseases by sex and presence of sarcopenia.

Muscle mass loss and fat mass increase are risk factors for cardiometabolic disease. We evaluated the effect of changes in body composition on the incidence of cardiometabolic diseases in older adults with or without sarcopenia, over two-year follow-up. Changes in body composition and the development of cardiometabolic diseases over 2years were measured in community-dwelling older adults recruited from the Korean Frailty Aging Cohort Study. Individuals with sarcopenia were 1:1 matched to those without sarcopenia via propensity score matching. Among a total of 1634 eligible subjects, 353 were identified with sarcopenia. In men without sarcopenia, an increase in waist circumference by 1cm was associated with a 32% higher risk of the development of hypertension. Conversely, an increase in appendicular lean mass by 1kg was associated with lower risks of the development of cardiovascular disease (41% lower) and hyperlipidemia (28% lower). However, there were no significant associations between changes in body composition and any incident cardiometabolic diseases in men with sarcopenia. Women without sarcopenia who experienced an increase in weight of 1kg were 21% less likely to develop hyperlipidemia. In women with sarcopenia, the risk of diabetes mellitus was reduced by 30% with an incremental increase in weight by 1kg, while the risk of hyperlipidemia increased almost threefold with an increase in appendicular lean mass by 1kg. In older adults without sarcopenia, a decrease in obesity-related indices and a gain in muscle gain are beneficial for men, but inverse relationships between weight and cardiometabolic diseases were reported in women. We found no cardiometabolic benefit of increasing lean mass in older adults with sarcopenia regardless of sex.

Cardiovascular protective effects of natural flavonoids on intestinal barrier injury.

Natural flavonoids may be utilized as an important therapy for cardiovascular diseases (CVDs) caused by intestinal barrier damage. More research is being conducted on the protective properties of natural flavonoids against intestinal barrier injury, although the underlying processes remain unknown. Thus, the purpose of this article is to present current research on natural flavonoids to reduce the incidence of CVDs by protecting intestinal barrier injury, with a particular emphasis on intestinal epithelial barrier integrity (inhibiting oxidative stress, regulating inflammatory cytokine expression, and increasing tight junction protein expression). Furthermore, the mechanisms driving intestinal barrier injury development are briefly explored, as well as natural flavonoids having CVD-protective actions on the intestinal barrier. In addition, natural flavonoids with myocardial protective effects were docked with ZO-1 targets to find natural products with higher activity. These natural flavonoids can improve intestinal mechanical barrier function through anti-oxidant or anti-inflammatory mechanism, and then prevent the occurrence and development of CVDs.