Calcium Homeostasis Research Articles

Investigating potential molecular mechanisms of antiepileptic drug-induced depression through network toxicology and molecular docking.

Investigating potential molecular mechanisms of antiepileptic drug-induced depression through network toxicology and molecular docking.

Toxic effects and transcriptome analysis of the early life stages of Larimichthys crocea exposed to the bloom-forming dinoflagellate Alexandrium tamarense.

Toxic effects and transcriptome analysis of the early life stages of Larimichthys crocea exposed to the bloom-forming dinoflagellate Alexandrium tamarense.

Emerging roles for microproteins as critical regulators of endoplasmic reticulum function and cellular homeostasis.

Emerging roles for microproteins as critical regulators of endoplasmic reticulum function and cellular homeostasis.

Ivabradine ameliorates doxorubicin-induced cardiotoxicity through improving mitochondrial function and cardiac calcium homeostasis.

Ivabradine ameliorates doxorubicin-induced cardiotoxicity through improving mitochondrial function and cardiac calcium homeostasis.

MICU1 is the nexus for CaV3.3 regulation of mitochondrial calcium, redox balance and chondrocyte viability.

MICU1 is the nexus for CaV3.3 regulation of mitochondrial calcium, redox balance and chondrocyte viability.

Serum and urine metabolite correlates of vitamin D supplementation in the Atherosclerosis Risk in Communities (ARIC) study.

Serum and urine metabolite correlates of vitamin D supplementation in the Atherosclerosis Risk in Communities (ARIC) study.

Disrupted balance: The impact of apheresis on calcium and magnesium metabolism.

Disrupted balance: The impact of apheresis on calcium and magnesium metabolism.

The characterization of uterine calcium transport and metabolism during eggshell calcification of hens laying high or low breaking strength eggshell.

The characterization of uterine calcium transport and metabolism during eggshell calcification of hens laying high or low breaking strength eggshell.

PH-modulated pea protein-β-glucan and carboxymethyl chitosan double-layer complex coacervate microcapsules: Efficient vitamin D3 encapsulation and functional fortification of surimi.

pH-modulated pea protein-β-glucan and carboxymethyl chitosan double-layer complex coacervate microcapsules: Efficient vitamin D3 encapsulation and functional fortification of surimi.

Impact of gender and reproductive states on diets and intestinal microbiota in Pratt's leaf-nosed bats (Hipposideros pratti).

Impact of gender and reproductive states on diets and intestinal microbiota in Pratt's leaf-nosed bats (Hipposideros pratti).

Long-term cumulative toxicity of low-dose lanthanum on nitrifying bacteria in partial nitrification process: Mechanism of disruption of intracellular calcium homeostasis

Long-term cumulative toxicity of low-dose lanthanum on nitrifying bacteria in partial nitrification process: Mechanism of disruption of intracellular calcium homeostasis

"Nano-calcium L-Aspartate enhances rice tolerance to arsenic toxicity by improving nitrogen metabolism, cell wall sequestration, and antioxidant system".

"Nano-calcium L-Aspartate enhances rice tolerance to arsenic toxicity by improving nitrogen metabolism, cell wall sequestration, and antioxidant system".

Role of IP3R2-Mediated mitochondrial calcium homeostasis in early hypoxic stress injury of retinal pigment epithelial cells.

Role of IP3R2-Mediated mitochondrial calcium homeostasis in early hypoxic stress injury of retinal pigment epithelial cells.

Is Vitamin D Deficiency a Cause of Refractory Benign Paroxysmal Positional Vertigo (BPPV)?

<b>Introduction:</b> Vitamin D is crucial for calcium metabolism, and its role in benign paroxysmal positional vertigo (BPPV) pathogenesis has been increasingly recognized. However, its impact on treatment resistance in BPPV patients remains unclear and understudied.<b>Aim:</b> This study investigated the association between treatment resistance in BPPV and various risk factors, including vitamin D deficiency, age, gender, and comorbidities.<b>Materials and methods:</b> A retrospective review of medical records was conductedon 122 patients diagnosed with BPPV at a tertiary care hospital between January2020 and January 2023. The diagnosis of BPPV was confirmed using clinical historyand positional tests, while serum 25-OH vitamin D levels were measured usingchemiluminescence immunoassay. Patients who required three or more canalithrepositioning maneuvers were considered treatment-resistant. Logistic regressionanalysis was employed to assess the impact of demographic and clinical factors onBPPV treatment resistance, and recurrence rates were evaluated over a one-yearfollow-up period.<b>Results:</b> Logistic regression revealed that male gender, comorbidities, and betahistine use were significantly associated with BPPV resistance (p < 0.05), while no significant relationship was found between vitamin D levels and treatment resistance or recurrence (p > 0.05). Recurrence was observed in 22.1% of patients during the follow- -up period, though this was not significantly related to vitamin D status.<b>Conclusions:</b> While previous studies suggested a potential link between vitamin Ddeficiency and BPPV recurrence, this study found no significant association betweenvitamin D deficiency and resistance along with the recurrence of BPPV. Instead, malegender, comorbidities (notably hypertension), and betahistine use were identified asrisk factors for requiring multiple maneuvers. The study raises questions about therole of vitamin D in BPPV pathophysiology and suggests that other clinical factorsmay have a greater influence on treatment outcomes.

Symptomatic hypocalcaemia after administration of denosumab and iron infusion in patients with normal and impaired renal function.

Osteoporosis and iron deficiency anaemia are common coexisting comorbidities in an ageing population. To facilitate timely administration of disease-modifying therapy, denosumab and iron infusions are often given concurrently on the day of discharge from an inpatient admission following fracture. It is becoming increasingly recognised that close administration of both can result in profound hypocalcaemia and/or hypophosphataemia due to disruption of calcium, phosphate and bone remodelling homeostasis. Our case series describes three cases of clinically significant, symptomatic hypocalcaemia in the setting of this potential drug-drug interaction, with symptoms including atraumatic femoral fracture, subacute cognitive decline and non-sustained ventricular tachycardia. While most previous case reports described hypocalcaemia in patients with advanced chronic kidney disease, two out of three of our cases had normal renal function, and one patient developed hypocalcaemia despite having calcium and cholecalciferol supplementation before and after denosumab administration. The optimal safe period between administration of the two medications has not been clearly established; one of our patients developed electrolyte disturbances despite having the medications 10 weeks apart.

Forward Engineering Organ Development and Cancer Therapeutics with Optogenetics.

Robust growth control is an essential requirement for the survival of living organisms, while its dysregulation results in diseases such as cancer. However, a significant knowledge gap exists in understanding how precise organ growth control is achieved. The growing arsenal of optogenetic toolkits allows precise, noninvasive control of cellular signaling in vivo, enabling research into how bioelectrical and chemical cues regulate organ growth. Here, we used the red-light-activated channelrhodopsin, CsChrimson, to stimulate intracellular calcium signaling dynamics in the wing epithelium of Drosophila melanogaster , an established model system for investigating organ size control. By varying light intensity and activation dynamics systematically, we identified a biphasic regulation of final organ size. Illumination of CsChrimson depolarizes cells and stimulates spikes of cytosolic calcium concentrations, a phenomenon explained by a computational model that incorporates the inclusion of both gap junction closure and voltage-gated calcium channel activation. This calcium regulation tunes downstream effectors involved in growth regulation and apoptosis. In particular, we found that prolonged bright red light exposure (100 lux/12 hours) increased cell death in wing imaginal discs and caused severe morphological abnormalities in adult wings, with phenotypic severity dependent on stimulation parameters defined by illumination intensity and period of activation. Strikingly, an optimum level of dim, pulsatile light (5 lux, 1 minute on/off pulse train) resulted in overgrown organs and significantly upregulated cell proliferation. We also co-expressed an oncogene, Ras V12 , with CsChrimson and showed that experimental optical simulation parameters can be exploited to control the morphology of tumorous tissues and initiate targeted remission of tumorous growth. Our findings and approach provide a powerful framework to dissect the role of dynamic physiological signaling events in organogenesis and offer translational insights into new therapeutic strategies with applications in cancer and regenerative medicine.

Coupling of Intracellular Calcium Homeostasis and Formation and Secretion of Matrix Vesicles: Their Role in the Mechanism of Biomineralization.

The human bone is a dynamic, highly vascularized tissue composed of 60-70% minerals, which include mainly calcium phosphate (CaP) in the form of hydroxyapatite (HA) crystals, 30% organic matrix composed of type I collagen fibers, and less than 5% water and lipids. The crystals are formed inside the matrix vesicles (MVs) and are then released in the organic collagen-based fibrous matrix. Extracellular matrix (ECM) formation and mineralization processes, named osteogenesis, are associated with human mesenchymal stem cells (hMSCs) undergoing differentiation into osteoblasts (osteoblastogenesis). Osteogenesis is regulated by multiple intracellular signaling and genetic pathways and by environmental factors. Calcium flow is finely regulated and plays a key role in both osteoblastogenesis and osteogenesis. The formation and accumulation of CaP, the biogenesis of MVs, their secretion, and the deposition of HA crystals to fill the organic bone matrix are the fundamental events in the biomineralization process. In this paper, I will describe and discuss the recent findings and hypothesis on the molecular mechanism regulating this process.

Genetic Predisposition and Mitochondrial Dysfunction in Sudden Cardiac Death: Role of MCU Complex Genetic Variations.

Sudden cardiac death (SCD) is a major cause of cardiovascular mortality, with coronary artery disease-related SCD (SCD-CAD) being the most prevalent form. Genetic factors and mitochondrial dysfunction, particularly in calcium homeostasis, are critical in SCD-CAD. However, the specific genetic factors linked to mitochondrial dysfunction in SCD-CAD remain poorly understood. In this case-control study, we analyzed 229 SCD-CAD cases and 598 controls from a Southern Han Chinese population, focusing on 12 insertion-deletion (indel) variants across six mitochondrial calcium uniporter (MCU) complex genes. We used capillary electrophoresis-based multiplex genotyping and performed logistic regression and haplotype analyses to assess the association of these variants with SCD-CAD susceptibility. Four significant indel variants and three risk-associated haplotypes were identified. Two of these indels were previously validated in the GWAS catalog as strongly linked to cardiac disorders. Additionally, Mendelian randomization (MR) analysis revealed a causal relationship between elevated levels of the SMDT1-encoded MCU regulator and increased risks of cardiovascular diseases, including coronary atherosclerosis, myocardial infarction, and cardiomyopathy. These findings highlight the role of MCU complex variants in SCD-CAD susceptibility and suggest their potential as biomarkers for cardiovascular risk stratification. Further research with larger cohorts is needed to confirm these results and explore underlying mechanisms.

Molecular Insight into the Role of Vitamin D in Immune-Mediated Inflammatory Diseases.

In the last decades, it has become increasingly evident that the role of vitamin D extends beyond the regulation of calcium homeostasis and the maintenance of bone health. A significant extraskeletal function of vitamin D is its role in modulating the immune system, particularly highlighted in the context of immune-mediated inflammatory diseases, where correlations between vitamin D status and genetic variations in the vitamin D receptor have been observed about the incidence and severity of these conditions. Additionally, different studies have reported the existence of immunomodulatory effects of vitamin D, particularly the effects of vitamin D on dendritic cell function, maturation, cytokine production, and antigen presentation, and that its deficiency may be associated with a sub-inflammatory state. In this sense, different clinical trials have been conducted to assess the therapeutic efficacy of vitamin D in different immune-mediated inflammatory disorders, including asthma, atopic dermatitis (AD), rheumatoid arthritis (RA), psoriasis, thyroid diseases, infectious diseases, and systemic lupus erythematosus (SLE). This review will provide a comprehensive overview of the current understanding of the molecular mechanisms underlying vitamin D's immunomodulatory properties, its role, and innovative therapeutic applications in patients with immune-mediated inflammatory diseases.

COMBINATION THERAPY WITH SEMAGLUTIDE AND DAPAGLIFLOZIN REDUCES SYNERGISTICALLY ANTHRACYCLINE–INDUCED CARDIOTOXICITY UNDER HYPERGLYCEMIA: IMPLICATIONS IN PRIMARY PREVENTION OF CTRCD IN CANCER PATIENTS WITH T2DM

COMBINATION THERAPY WITH SEMAGLUTIDE AND DAPAGLIFLOZIN REDUCES SYNERGISTICALLY ANTHRACYCLINE–INDUCED CARDIOTOXICITY UNDER HYPERGLYCEMIA: IMPLICATIONS IN PRIMARY PREVENTION OF CTRCD IN CANCER PATIENTS WITH T2DM