Angiotensin-converting Enzyme Research Articles

Angiotensin-Converting Enzyme 2 in AKI Was Attenuated by Uremia Toxin Indoxyl Sulfate and Restored by Renin-Angiotensin-Aldosterone System Inhibitors

Angiotensin-Converting Enzyme 2 in AKI Was Attenuated by Uremia Toxin Indoxyl Sulfate and Restored by Renin-Angiotensin-Aldosterone System Inhibitors

Exogenous Angiotensin-(1-7) Provides Protection Against Inflammatory Bone Resorption and Osteoclastogenesis by Inhibition of TNF-α Expression in Macrophages.

Renin-angiotensin-aldosterone system plays a crucial role in the regulation of blood pressure and fluid homeostasis. It is reported to be involved in mediating osteoclastogenesis and bone loss in diseases of inflammatory bone resorption such as osteoporosis. Angiotensin-(1-7), a product of Angiotensin I and II (Ang I, II), is cleaved by Angiotensin-converting enzyme 2 and then binds to Mas receptor to counteract inflammatory effects produced by Ang II. However, the mechanism by which Ang-(1-7) reduces bone resorption remains unclear. Therefore, we aim to elucidate the effects of Ang-(1-7) on lipopolysaccharide (LPS)-induced osteoclastogenesis. In vivo, mice were supracalvarial injected with Ang-(1-7) or LPS ± Ang-(1-7) subcutaneously. Bone resorption and osteoclast formation were compared using micro-computed tomography, tartrate-resistant acid phosphatase (TRAP) stain, and real-time PCR. We found that Ang-(1-7) attenuated tumor necrosis factor (TNF)-α, TRAP, and Cathepsin K expression from calvaria and decreased osteoclast number along with bone resorption at the suture mesenchyme. In vitro, RANKL/TNF-α ± Ang-(1-7) was added to cultures of bone marrow-derived macrophages (BMMs) and osteoclast formation was measured via TRAP staining. The effect of Ang-(1-7) on LPS-induced osteoblasts RANKL expression and peritoneal macrophages TNF-α expression was also investigated. The effect of Ang-(1-7) on the MAPK and NF-κB pathway was studied by Western blotting. As a result, Ang-(1-7) reduced LPS-stimulated macrophages TNF-α expression and inhibited the MAPK and NF-κB pathway activation. However, Ang-(1-7) did not affect osteoclastogenesis induced by RANKL/TNF-α nor reduce osteoblasts RANKL expression in vitro. In conclusion, Ang-(1-7) alleviated LPS-induced osteoclastogenesis and bone resorption in vivo via inhibiting TNF-α expression in macrophages.

Seven-tesla magnetic resonance imaging of the nervus terminalis, olfactory tracts, and olfactory bulbs in COVID-19 patients with anosmia and hypogeusia.

Linking olfactory epithelium to the central nervous system are cranial nerve 1, the olfactory nerve, and cranial nerve "0," and the nervus terminalis (NT). Since there is minimal expression of angiotensin-converting enzyme-2 (ACE-2) in the olfactory nerve, it is unclear how SARS-CoV-2 causes anosmia (loss of smell) and hypogeusia (reduction of taste). In animal models, NT expresses ACE-2 receptors, suggesting a possible SARS-CoV-2 viral entry site in humans. The purpose of this study was to determine whether ultra-high-field 7 T magnetic resonance imaging (MRI) could visualize the NT, olfactory bulbs (OB), and olfactory tract (OT) in healthy controls and COVID-19 anosmia or hypogeusia and to qualitatively assess for volume loss and T2 alterations. In this study, 7 T MRI was used to evaluate the brain and olfactory regions in 45 COVID-19 patients and 29 healthy controls. Neuroimaging was qualitatively assessed by four board-certified neuroradiologists who were blinded to outcome assignments: for the presence or absence of NT; for OB, OT, and brain volume loss; and altered T2 signal, white matter T2 hyperintensities, microhemorrhages, enlarged perivascular spaces, and brainstem involvement. NT was identifiable in all COVID-19 patients and controls. T2 hyperintensity in the NT, OB, and OT in COVID-19 patients with anosmia or hypogeusia was statistically significant compared to controls and COVID-19 patients without anosmia or hypogeusia. On 7 T MRI, NT was radiographically identifiable, adjacent to OB and OT. In COVID-19 anosmia and hypogeusia, T2 hyperintensity of NT, OB, and OT was statistically significant compared to COVID-19 patients without anosmia or hypogeusia and controls. The NT may be a potential entry site for SARs-CoV-2 and may play a role in the pathophysiology of COVID-19 anosmia.

Unveiling the Dynamic Mechanism of SARS-CoV-2 Entry Host Cells at the Single-Particle Level.

Understanding the dynamic features of severe acute respiratory coronavirus 2 (SARS-CoV-2) binding to the cell membrane and entry cells is crucial for comprehending viral pathogenesis and transmission and facilitating the development of effective drugs against COVID-19. Herein, we employed atomic force microscopy (AFM)-based single-molecule force spectroscopy (SMFS) to study the binding dynamics between the virus and cell membrane. Our findings revealed that the Omicron variant of SARS-CoV-2 virus-like particles (VLPs) exhibited a slightly stronger affinity for the angiotensin-converting enzyme-2 (ACE2) receptor compared with the Delta variant and was significantly higher than the wild-type (WT). Using a real-time force-tracing technique, we quantified the dynamic parameters for a single SARS-CoV-2 VLP entry into cells, showing that approximately 200 ms and 60 pN are required. The parameters aligned with the analysis obtained from coarse-grained molecular dynamics (CGMD) simulations. Additionally, the Omicron variant invades cells at a higher entry cell speed, smaller force, and higher probability. Furthermore, single-particle fluorescence tracking visually demonstrated clathrin-dependent endocytosis for SARS-CoV-2 entry into A549 cells. The dynamic features of endocytosis provide valuable insights into the SARS-CoV-2 entry mechanism and possible intervention strategies targeting the viral infection process.

Assessment of the influence of body fat indices on antihypertensive drug responses.

Less than 50% of patients treated for hypertension reach a target office systolic blood pressure (SBP). We aimed to evaluate the role of adiposity on antihypertensive drug responses in newly diagnosed hypertensive patients. Estimated glomerular filtration rates, body mass index (BMI), skinfold thickness (SFT), body surface areas and waist circumferences of 150 hypertensive patients naïve to treatment were measured. Treatment protocols were started as combination of angiotensin converting enzyme inhibitor (ACE-I) plus calcium channel blocker (CCB), angiotensin receptor blocker plus CCB or ACE-I plus diuretic. Pre-treatment and change in blood pressure (ΔBP) after 4weeks treatment were determined. Multiple linear regression analysis was used to find independent predictors of Δblood pressure changes, and multivariable binary logistic regression analysis to find independent predictors of target SBP < 140 mmHg at 4weeks. A total of 104 patients reached the target systolic pressure of <140 mmHg at 4weeks. Triceps, mid-abdomen and subscapular SFT were significantly thicker in the uncontrolled blood pressure group (P = .011, P = .006 and P = .016, respectively). Pretreatment SBP (r = 0.644), pretreatment diastolic blood pressure (DBP) (r = 0.188), subscapular SFT (r = -0.318), suprailiac SFT (r = -0.211) and ΔDBP (r = 0.433) were correlated with ΔSBP in correlation analysis. Pretreatment SBP (β = 0.644, 95% CI = 0.697-0.993, P < .001), subscapular SFT (β = -0.253, 95% CI = -0.886--0.329, P < .001), pretreatment DBP (β = -0.380, 95% CI = -0.1001- -0.453, P = .001) and ΔDBP (β = 0.401, 95% CI = 0.377-0.796, P < .001) were independent predictors of ΔSBP in multivariable linear regression analysis. Subscapular SFT was an independent predictor of target SBP < 140 mmHg in multivariable logistic regression analysis (OR = 0.895, 95% CI = 0.832-0.963, P = .003). Subscapular SFT may be a valuable marker for prediction of response to antihypertensive drugs.

Protocolo terapéutico de la diabetes mellitus tipo 2 con nefropatía

The protocol describes the therapeutic management of patients with type 2 diabetes mellitus (DM2) and chronic kidney disease (CKD), a frequent complication in 20%–40% of individuals with DM2. Treatment is based on blood pressure control (target<130/80mmHg); angiotensin-converting enzyme inhibitors (ACE inhibitors) or angiotensin II receptor blockers (ARBs) are recommended. For glycemic control, the glycosylated hemoglobin (HbA1c) level sought is individualized for each patient, but is generally below 7%, adjusting the medication according to the patient's estimated glomerular filtration rate (eGFR). Sodium-glucose cotransporter-2 (SGLT-2i) inhibitors and glucagon-like peptide-1 agonists (GLP-1a) are recommended for their renal and cardiovascular benefits. In addition, patients with CKD and DM2 should be treated with statins to reduce cardiovascular risk, avoiding drugs that increase the risk of hypoglycemia. Individualized treatment and frequent monitoring are essential, especially in patients with decreased eGFR and persistent albuminuria.

Effect of calcium channel blockers on influenza incidence: a population-based retrospective cohort study using administrative claims data in Japan

ObjectivesLaboratory experiments have indicated that calcium channel blockers (CCBs) inhibit the entry and replication of influenza A virus in cells. However, no clinical studies have assessed the incidence of influenza...

Exploring the nutritional and biological properties of green coffee extracts: A comparative study of aqueous and enzymatic extraction processes

The effects of aqueous (AEP) and enzyme-assisted aqueous extraction processes (EAEP) on the biological and nutritional properties of green coffee extracts (protein and antioxidant-rich fraction) were investigated. All extracts exhibited high in vitro protein digestibility (>98%), regardless of the pH and use of enzymes during extraction, probably due to the low molecular weight of coffee proteins. Raising extraction pH from 7.0 to 9.0 resulted in extracts with lower concentrations of caffeine and some phenolic compounds such as chlorogenic and cinnamic acids, as well as catechin and epicatechin. This led to a reduction in the antioxidant activity of the extracts obtained at alkaline pH (AEP – pH 9.0). Overall, higher phenolic and caffeine extractability was achieved at neutral pH (AEP – pH 7.0), with no observed improvement in extraction yields when carbohydrases and/or proteases were employed. Coffee extracts generated by AEP at pH 7.0 exhibited the highest lipase inhibitory activity (66%), primarily attributed to their higher chlorogenic acid concentration. Conversely, EAEP extracts exhibited higher angiotensin-converting enzyme inhibition (up to 85%) compared to AEP extracts (68.5 – 74.3%). This strong inhibitory activity is likely related to the presence of both phenolic compounds (mainly chlorogenic acid) and smaller peptides. Nevertheless, all extracts exhibited low effectiveness for α-glucosidase inhibition (≤14%) and antimicrobial activity against S. aureus and E. coli. The current research underscores the feasibility of modulating the composition of green coffee extracts using sustainable and scalable AEP and EAEP, paving the way for developing tailored extracts with specific biological properties.

In advanced CKD, ACEis or ARBs reduce kidney failure vs. placebo or non-RAAS inhibitors at 34 mo.

Ku E, Inker LA, Tighiouart H, et al. Angiotensin-converting enzyme inhibitors or angiotensin-receptor blockers for advanced chronic kidney disease: a systematic review and retrospective individual participant-level meta-analysis of clinical trials. Ann Intern Med. 2024;177:953-963. 38950402.

Association of the Polymorphisms of the Angiotensin-Converting Enzyme and FRMD3 Genes in the Development of Diabetic Kidney Disease

Association of the Polymorphisms of the Angiotensin-Converting Enzyme and FRMD3 Genes in the Development of Diabetic Kidney Disease

The Canadian Heart Failure (CAN-HF) Registry: A Canadian Multicentre, Retrospective Study of Outpatients with Heart Failure

BackgroundGuideline-directed medical therapy (GDMT) reduces events in patients with heart failure (HF) with reduced ejection fraction (HFrEF). Despite this impact, underutilization of GDMT persists. This report sought to describe HF management in Canadian outpatients treated at specialized HF clinics (HFCs). MethodsThe Canadian Heart Failure (CAN-HF) study was retrospective and observational, and it included 1775 patients from 6 Canadian outpatient HFCs, from the period January 2017-April 2020. ResultsWe observed improvement in prescription rates in patients with HFrEF, between their first visit and their most-recent clinic visit, across all GDMT classes, in those who were followed at the HFC for ≥ 6 months. The largest prescription rate increases were observed for angiotensin receptor–neprilysin inhibitors and mineralocorticoid-receptor antagonists. However, more than half of the patients remained on angiotensin-converting enzyme inhibitors and/or angiotensin-receptor blockers, despite being symptomatic, according to their New York Heart Association class. Most patients (50%) were on triple therapy, as of their most-recent visit, with fewer (36%) on dual therapy, monotherapy (13%), or no GDMT (2%). Our data also suggest that patients who had been managed at the HFC for > 6 months had higher prescription rates of GDMT and were on higher doses of GDMT, compared to those who were new to the clinic. For patients with HF with preserved ejection fraction, few patients were on candesartan and less than half were on a mineralocorticoid-receptor antagonist. ConclusionsOur data from HFCs that in most cases were affiliated with academic centres compare favourably with data from other analyses of ambulatory patients with HFrEF, evidence that supports the use of a specialized patient-care model.

The delapril-indapamide combination in treatment of arterial hypertension: practical implications in light of the new guidelines.

The recent guidelines issued by the European Society of Hypertension reaffirmed that the degree of control of hypertension remains suboptimal worldwide. In order to increase the proportion of well-controlled patients, in addition to nonpharmacological measures, it is necessary to improve the implementation of drug therapy in the clinical practice as much as possible. Initial therapy should almost always be based on the combination, free or fixed, between ACE inhibitor drugs, or direct angiotensin II inhibitors ('sartans') and diuretics (thiazide or thiazide-like) or calcium channel blockers at the maximum recommended and well-tolerated dose. The combination of the thiazide-like diuretic indapamide with the ACE inhibitor delapril has shown, based on numerous clinical trials and meta-analyses, very good results in terms of antihypertensive efficacy, tolerability, and prevention or regression of organ damage. Indapamide is a thiazide-like diuretic also endowed with direct vasodilator effect and long duration of action. A meta-analysis of 19 randomized clinical trials demonstrated a greater reduction in the incidence of cardiac events, stroke and heart failure with thiazide-like diuretics than with thiazide diuretics. Delapril is a non-sulfhydryl ACE-inhibitor with high affinity for converting enzyme at the cardiac, pulmonary, and peripheral vascular levels. Being strongly lipophilic, delapril inhibits the ACE enzyme at the tissue level more potently than other ACE inhibitors. A peculiar feature of delapril is its weak bradykinin-enhancing effect due to its higher affinity for the C site than the N site of ACE, resulting in a lower incidence of cough and angioneurotic edema compared with other ACE inhibitors. In some meta-analyses, the pressor reduction was statistically, greater with the delapril-indapamide combination than with combinations between hydrochlorothiazide and ACE inhibitors. The combination consists of divisible tablets containing 30 mg delapril and 2.5 mg indapamide, and its pharmacological and clinical properties are not affected by simultaneous food intake. The antihypertensive efficacy of the combination, as well as its components, persists for the entire 24 hours. The recent alarming reports on the incidence of skin cancer during treatment with hydrochlorothiazide should also be a guide in clinical practice toward the preferential choice of a thiazide-like diuretic such as chlorthalidone or indapamide to replace hydrochlorothiazide.

High fat, high sucrose diet promotes increased expression of ACE2 receptor in the SIV-infected host: implications for SARS-CoV-2 infection.

People with pre-existing conditions, including metabolic comorbidities, are at greater risk for complications of SARS-CoV-2 infection and expression of machinery required for viral entry into host cells may be a contributing factor. This study tested the hypothesis that high fat, high sucrose diet (HFSD) and alcohol use increase expression of angiotensin converting enzyme 2 (ACE2) receptor and transmembrane serine protease 2 (TMPRSS2) in tissues isolated from simian immunodeficiency virus (SIV) infected macaques, the most clinically relevant model for the study of HIV. Biospecimens obtained from a longitudinal study of SIV-infected, antiretroviral therapy (ART)-treated female rhesus macaques (Macaca mulatta) were used to determine whether HFSD and chronic binge alcohol (CBA) increased ACE2 and TMPRSS2 protein and gene expression. Macaques (n = 10) were assigned to HFSD or standard diet (SD) for 3 months before CBA or vehicle administration. Three months later, macaques were infected with SIV; ART was initiated 2.5 months thereafter. Tissue samples including lung, pancreas, and kidney were collected at study endpoint (12 months post-SIV infection). Protein expression of ACE2 in the lung, whole pancreas, and pancreatic islets was significantly greater in HFSD- than SD-fed macaques with no significant differences in protein expression of TMPRSS2 or mRNA expression of ACE2 or TMPRSS2. CBA did not significantly alter any measures. The increased ACE2 receptor expression observed in lung and pancreas of SIV-infected HFSD-fed female rhesus macaques aligns with reports that diet may increase susceptibility to COVID-19. These data provide direct evidence for a link between dietary quality and cellular adaptations that may increase the risk for SARS-CoV-2 infection.

Study of biomarkers to determine severity and lung damages in COVID-19 patients.

Identifying inflammation and lung damage markers is crucial in reducing morbidity and mortality of coronavirus disease 2019 (COVID-19). This study aimed to examine the validity and reliability of severity and post-infection lung damage and analyse their relationship. This was a prospective analysis study at the Airlangga University Hospital, Surabaya, Indonesia, from March to August 2021. The infection`s severity was measured by examining angiotensin-converting enzyme 2 (ACE2) levels and complete blood count. Lung damage was estimated by reviewing Krebs von de Lungen (KL)-6, matrix metalloproteinase (MMP)-9, tissue inhibitor metalloproteinase (TIMP)-1, and MMP-9/TIMP-1. Two-factor confirmatory factor analysis (CFA) and canonical correlation were calculated using Lisrel and SPSS (version 25). The research sample included 76 patients. The t count loading factor values were calculated: ACE2 (6.00), neutrophils (-0.80), lymphocytes (-0.63), neutrophil-lymphocyte ratio (NLR, 1.27), eosinophils (-1.52), basophils (1.72), monocytes (0.05), platelets (0.53), leukocytes (-0.51), platelet-lymphocyte ratio (PLR, -1.15), KL-6 (10.47), MMP-9 (11.91), TIMP-1 (11.79), and MMP-9/TIMP-1 (-0.24). The t values were: neutrophil covariance error (6.11), lymphocytes (6.12), NLR (6.10), eosinophils (6.08), basophils (6.07), monocytes (6.12), platelets (6.12), leukocytes (6.12), PLR (6.10), ACE2 (0.97), KL-6 (5.63), MMP-9 (2.08), TIMP-1 (2.77), and MMP-9/TIMP-1 (6.12). t value canonical correlation of 7.04 (t count > 1.96) indicated a correlation between the severity of the patient and post-infection lung damage. The severity was adequately measured through ACE2, IL-6, IL-10, neutrophils, lymphocytes, leukocytes, and NLR. Lung damage was measured with KL-6, MMP-9, and TIMP-1. There was a correlation between disease severity and lung damage.

Frequency of rs35803318 single nucleotide polymorphism of ACE2 gene among the Kazakhs

In the article the results of genotyping of DNA samples obtained from the study participants on the single nucleotidepolymorphism (SNP) rs35803318 (C/T) of the ACE2 gene were presented. Genotyping was carriedout by real-time polymerase chain reaction (PCR) using the technique Amplification of the Refractory MutationSystem (ARMS). The frequencies of rs35803318 (C/T) genotypes and alleles in 96 representatives of theKazakh ethnic group living in the Karaganda region were analyzed. The ACE2 gene (angiotensin-convertingenzyme 2) was extensively investigated due to its role in susceptibility to infection by the SARS-CoV-2 viruscausing COVID-19. The ACE2 gene encodes a protein that serves as a receptor for the virus, and its variationscan affect a person's susceptibility to infection. The ACE2 protein plays a role in the regulation of angiotensinand the effect on blood pressure. Therefore, there is a link between ACE2 gene polymorphisms, includingrs35803318, and the development of cardiovascular diseases. According to the results of our study,the CT genotype (63.5 %) is the most common among Kazakhs, the CC genotype was 20.8 % and theTT genotype was 15.6 %. The distribution of polymorphism alleles is as follows: allele C — 52.6 %, allele A— 47.4 %.

A Comprehensive Examination of the Association Between the ACE2 Gene with the Susceptibility to COVID-19 and the Occurrence of Diabetes Mellitus

Background: The rate of transmission, as well as the risk of death associated with COVID-19, is significantly higher than that of previous epidemics. Among the underlying health conditions frequently observed in affected populations, diabetes stands out as one of the most prevalent. Individuals with diabetes who contract Covid-19 face a heightened risk of disease progression compared to those with other conditions. Materials and Methods: A case-control study was implemented to assess biomarkers using classical lab work procedures and genetic markers using congenital PCR, then the association between ACE2 gene, COVID-19 and Diabetes Mellitus were implemented. Results: The analysis of the ACE2 (ID; DD) group revealed statistically significant differences between the groups. However, the II as well as I groups did not demonstrate any notable differences. The chi-square method employed, with a p-value set at &lt; 0.05, indicating statistical significance. Among the manage organization, those with covid-19 , and humans with diabetes plus covid19, the ACE2 D genotype was the most common genotype, accounting for 72.6%, 85%, and 54% of the full population, respectively. After this, the DD, ID, and I genotypes have been applied to the samples. Conclusions: The ACE2 D genotype showed significant prevalence in COVID-19 and diabetes populations, while the II and I genotypes showed no notable differences, highlighting ACE2 D’s potential importance

Novel Bioactive Peptides from Red Bigeye (Priacanthus macracanthus) Flesh Protein

Red bigeye (Priacanthus macracanthus) is a common fish species in Malaysia. This study reported an in silico assessment of the main proteins in red bigeye flesh as precursors for bioactive peptides. Six major proteins were chosen as precursors from the proteomic profiles of red bigeye proteins. Analyses using the BIOPEP-UWM database found that Protein number 4 gave the highest total number of bioactive peptides (5052 peptides), with dominant bioactivity in angiotensin-I-converting enzyme (ACE) inhibition (1571 peptides) and dipeptidyl peptidase-IV (DPP-IV) inhibition (2238 peptides). The ACE inhibitors had a frequency of bioactive fragment occurrences (A) of 0.4098, while the DPP-IV inhibitors gave a frequency of 0.5805. In silico proteolysis using BIOPEP-UWM found that pepsin (pH &gt; 2) was the most promising proteinase in releasing a high number of DPP-IV and ACE inhibitory peptides. A novel peptide with significant potential was identified as QYKF. This study shows that red bigeye is a potential source of antihypertensive and antidiabetic peptides.

Could Timed Targeting of the Circadian-Controlled NLRP3 Inflammasome Be a Potential Therapeutic Strategy for Treatment of COVID-19–Induced Encephalitis?

The new coronavirus disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has several manifestations including neurological complications like encephalitis. The NOD-like receptor family pyrin domain-containing 3 (NLRP3) inflammasomes, which are regulated by the circadian clock genes, are key signaling proteins that detect pathogenic microorganisms and sterile stressors and activate the pro-inflammatory cytokines such as interleukin-1β and -18 (IL-1β and IL-18). The disruption of circadian rhythms following SARS-CoV-2 binding to angiotensin-converting enzyme 2 (ACE2) receptors in the capillary endothelium could lead to hyperactivation of the NLRP3 inflammasome, contributing to an enhanced inflammatory response in the central nervous system, thereby increasing susceptibility to or severity of coronavirus disease 2019 (COVID-19)-induced encephalitis. This review highlights the role of the circadian-controlled NLRP3 inflammasome in the pathogenesis of COVID-19-induced encephalitis and suggests targeting the NLRP3 circadian axis for timely intervention as a potential therapeutic target for the treatment of COVID-19-induced encephalitis.

From Sea to Lab: Angiotensin I-Converting Enzyme Inhibition by Marine Peptides-Mechanisms and Applications.

To reveal potent ACE inhibitors, researchers screen various bioactive peptides from several sources, and more attention has been given to aquatic sources. This review summarizes the recent research achievements on marine peptides with ACE-inhibitory action and application. Marine peptides are considered excellent bioactives due to their large structural diversity and unusual bioactivities. The mechanisms by which these marine peptides inhibit ACE include competitive binding to ACEs' active site, interfering with ACE conformational changes, and avoiding the identification of substrates. The unique 3D attributes of marine peptides confer inhibition advantages toward ACE activity. Because IC50 values of marine peptides' interaction with ACE are low, structure-based research assumes that the interaction between ACE and peptides increased the therapeutic application. Numerous studies on marine peptides focused on the sustainable extraction of ACE-inhibitory peptides produced from several fish, mollusks, algae, and sponges. Meanwhile, their potential applications and medical benefits are worth investigating and considering. Due to these peptides exhibiting antioxidant, antihypertensive, and even antimicrobial properties simultaneously, their therapeutic potential for cardiovascular disease and other illnesses only increases. In addition, as marine peptides show better pharmacological benefits, they have increased absorption rates and low toxicity and could perhaps be modified for better stability and bioefficacy. Biotechnological advances in peptide synthesis and formulation have greatly facilitated the generation of peptide-based ACE inhibitors from marine sources, which subsequently offer new treatment models. This article gives a complete assessment of the present state of knowledge about marine organism peptides as ACE inhibitors. In addition, it emphasizes the relevance of additional investigation into their mechanisms of action, the optimization of manufacturing processes, and assessment in in vivo, preclinical, and clinical settings, underlining the urgency and value of this study. Using marine peptides for ACE inhibition not only broadens the repertory of bioactive compounds but also shows promise for tackling the global health burden caused by cardiovascular diseases.

Design and cohort characteristics of TRACK, a prospective study of hyperkalaemia management decision-making.

Guideline-recommended hyperkalaemia management includes dietary potassium (K+) restriction, bicarbonate correction, diuretics and K+ binders with dose reduction of renin-angiotensin-aldosterone system inhibitors as a last resort. The extent to which these recommendations are implemented is uncertain, as real-world data on hyperkalaemia management are limited. The Tracking Treatment Pathways in Adult Patients with Hyperkalemia (TRACK) study is a multinational, prospective, longitudinal study that is being conducted to address this knowledge gap. We report the design and baseline cohort characteristics of this real-world study of hyperkalaemia management decision-making. This study enrolled participants within 21days of an episode of hyperkalaemia in four European countries (UK, Spain, Germany, Italy) and the USA. During the 12-month follow up, data collected will include participant and healthcare provider characteristics (specialty and practice setting), hyperkalaemia treatment objectives and strategies, rationale for management decisions and indicators of response and patient-reported perceptions of their hyperkalaemia treatment. The enrolled cohort includes 1330 participants, mean age 68years, of whom 31% were women. At baseline, 6% reported heart failure, 55% chronic kidney disease, 29% both and 9% neither. Most participants (57%) were taking an angiotensin-converting enzyme inhibitor, angiotensin receptor blocker or angiotensin receptor/neprilysin inhibitor at baseline. Mineralocorticoid receptor antagonist use was lower (14%). The prospective TRACK study will shed light on practitioners' hyperkalaemia management decision-making and assess the impact of their decisions on hyperkalaemia recurrence. Understanding practitioners' underlying thought processes will facilitate efforts to improve hyperkalaemia management.ClinicalTrials.gov: NCT05408039.