With aging, there is a decline in cardiac function accompanying increasing risk of arrhythmias. These effects are likely to be mechanistically associated with age-associated changes in calcium regulation within cardiac myocytes. Previous studies suggest that lifelong exercise can potentially reduce age-associated changes in the heart. Although exercise itself is associated with changes in cardiac function, little is known about the interactions of aging and exercise with respect to myocyte calcium regulation. To investigate this, adult (12 months) and old (24 months) C57/Bl6 mice were trained using moderate-intensity treadmill running. In response to 10 weeks' training, comparable cardiac hypertrophic responses were observed, although aging independently associated with additional cardiac hypertrophy. Old animals also showed increased L- and T-type calcium channels, the sodium-calcium exchange, sarcoendoplasmic reticulum calcium ATPase, and collagen (by 50%, 92%, 66%, 88%, and 113% respectively). Short-term exercise training increased D-type and T-type calcium channels in old animals only, whereas an increase in sodium-calcium exchange was seen only in adult animals. Long-term (12 months) training generally opposed the effects of aging. Significant hypertrophy remained in long-term trained old animals, but levels of sarcoendoplasmic reticulum calcium ATPase, sodium-calcium exchange, and collagen were not significantly different from those found in the adult trained animals.
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http://dx.doi.org/10.1093/gerona/glv093 | DOI Listing |
Cardiovasc Toxicol
January 2025
Graduate Institute of Clinical Medicine, College of Medicine, Taipei Medical University, No. 250, Wuxing St., Taipei, 11031, Taiwan.
Ventricular arrhythmias (VAs) are major causes of sudden cardiac death in chronic kidney disease (CKD) patients. Indoxyl sulfate (IS) is one common uremic toxin found in CKD patients. This study investigated whether IS could induce VAs via increasing right ventricular outflow tract (RVOT) arrhythmogenesis.
View Article and Find Full Text PDFCurr Probl Cardiol
January 2025
Department of Cardiology, Lanzhou University Second Hospital, Lanzhou, China. Electronic address:
Atrial fibrillation (AF) is tightly linked to mitochondrial dysfunction, calcium (Ca²⁺) imbalance, and oxidative stress. Mitochondrial Ca²⁺ is essential for regulating metabolic enzymes, maintaining the tricarboxylic acid (TCA) cycle, supporting the electron transport chain (ETC), and producing ATP. Additionally, Ca²⁺ modulates oxidative balance by regulating antioxidant enzymes and reactive oxygen species (ROS) clearance.
View Article and Find Full Text PDFBiomed Pharmacother
January 2025
Department of Biology, University of Naples Federico II, Naples, Italy; Biogem, Istituto di Biologia e Genetica Molecolare, Ariano Irpino, AV, Italy.
Intracellular Ca homeostasis dysregulation, through the modulation of calcium permeable ion channels and transporters, is gaining attention in cancer research as an apoptosis evasion mechanism. Recently, we highlighted a prognostic role for several calcium permeable channels. Among them, here, we focused on the plasma membrane bidirectional Na/Ca exchanger SLC8A1.
View Article and Find Full Text PDFCell Calcium
January 2025
Cardiac Signaling Center of USC, MUSC and Clemson University, 68 President St BEB 306, Charleston, SC 29425, USA. Electronic address:
Rationale & Methods: While signaling of cardiac SR by surface membrane proteins (I & I) is well studied, the regulation of mitochondrial Ca by plasmalemmal proteins remains less explored. Here we have examined the signaling of mitochondria and SR by surface-membrane calcium-transporting proteins, using genetically engineered targeted fluorescent probes, mito-GCamP6 and R-CEPIA1er.
Results: In voltage-clamped and TIRF-imaged cardiomyocytes, low Na induced SR Ca release was suppressed by short pre-exposures to ∼100 nM FCCP, suggesting mitochondrial Ca contribution to low Na triggered SR Carelease.
Biosci Rep
December 2024
University of Lincoln College of Science, Lincoln, United Kingdom.
Cellular Ca2+ homeostasis is critical for normal cell physiology and is regulated by several mechanisms. Two major players in intracellular Ca2+ homeostasis in multiple tissues belong to SLC8 (Na+/Ca2+ exchangers (NCXs); NCX1-3) and SLC24 (K+ dependent Na+/Ca2+ exchangers (NCKXs); NCKX1-5) families. It has been established that NCXs and NCKX4 are palmitoylated, and that palmitoylation promotes NCX1 inactivation.
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