ArticleScientific reports2014
Functional role of Calstabin2 in age-related cardiac alterations.
Article in Scientific reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers, 1 of them a synthesis that pooled it.
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Who cites it
52 citing papers in PubMed, 1 synthesis or guideline pooled it, 68 citations in OpenAlex.
- Interplay between frailty and cardiometabolic disorders: from pathophysiology to clinical implications.Cardiovascular diabetology · 2025Pooled it
- Aberrant myocardial calcium cycling: pathogenic mechanisms and targeted therapeutics for heart failure.Frontiers in cardiovascular medicine · 2026Review
- Telomeric autophagy in human health, aging, and diseases.Frontiers in molecular biosciences · 2026Review
- Knockdown of FKBP12.6 may Cause Bladder Dysfunction in Mice by Affecting IP3R/TRPM4 Function.Current medicinal chemistry · 2026Article
- Statins, skeletal muscle, and ryanodine receptor activation: resolving a 30-year mystery behind statin myotoxicity.Cardiovascular diabetology. Endocrinology reports · 2025Article
- Doxorubicin induces cardiotoxicity by enhancing autophagy via mTOR signaling in hiPSC- and hESC-derived cardiomyocytes.Frontiers in cell and developmental biology · 2025Article
- The Impact of Vitamin E Supplementation on Oxidative Stress, Cognitive Functions, and Aging-Related Gene Expression in Aged Mice.Food science & nutrition · 2024Article
- Dysfunctional mitochondria elicit bioenergetic decline in the aged heart.The journal of cardiovascular aging · 2024Article
- Comprehensive machine learning models for predicting therapeutic targets in type 2 diabetes utilizing molecular and biochemical features in rats.Frontiers in endocrinology · 2024Article
- Article
- NADPH Oxidases and Oxidative Stress in the Pathogenesis of Atrial Fibrillation.Antioxidants (Basel, Switzerland) · 2023Review
- Mitochondrial Calcium Overload Plays a Causal Role in Oxidative Stress in the Failing Heart.Biomolecules · 2023Review
- Distinct signatures on d-galactose-induced aging and preventive/protective potency of two low-dose vitamin D supplementation regimens on working memory, muscular damage, cardiac and cerebral oxidative stress, and SIRT1 and calstabin2 downregulation.Food science & nutrition · 2023Article
- Dantrolene inhibition of ryanodine channels (RyR2) in artificial lipid bilayers depends on FKBP12.6.The Journal of general physiology · 2023Article
- miR-181c targets Parkin and SMAD7 in human cardiac fibroblasts: Validation of differential microRNA expression in patients with diabetes and heart failure with preserved ejection fraction.Mechanisms of ageing and development · 2023Article
- SGLT2 Inhibition via Empagliflozin Improves Endothelial Function and Reduces Mitochondrial Oxidative Stress: Insights From Frail Hypertensive and Diabetic Patients.Hypertension (Dallas, Tex. : 1979) · 2022Article
- Role of oxidation of excitation-contraction coupling machinery in age-dependent loss of muscle function ineLife · 2022Article
- IP3 receptor orchestrates maladaptive vascular responses in heart failure.The Journal of clinical investigation · 2022Article
- Ion Channels and Transporters in Autophagy.Autophagy · 2022Article
- Functional role of miR-34a in diabetes and frailty.Frontiers in aging · 2022Review
Corrections and comments
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Authors and funding
11 authors at 6 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Calstabin2 is a component of the cardiac ryanodine receptor (RyR2) macromolecular complex, which modulates Ca(2+) release from the sarcoplasmic reticulum in cardiomyocytes. Previous reports implied that genetic deletion of Calstabin2 leads to phenotypes related to cardiac aging. However, the mechanistic role of Calstabin2 in the process of cardiac aging remains unclear. To assess whether Calstabin2 is involved in age-related heart dysfunction, we studied Calstabin2 knockout (KO) and control wild-type (WT) mice. We found a significant association between deletion of Calstabin2 and cardiac aging. Indeed, aged Calstabin2 KO mice exhibited a markedly impaired cardiac function compared with WT littermates. Calstabin2 deletion resulted also in increased levels of cell cycle inhibitors p16 and p19, augmented cardiac fibrosis, cell death, and shorter telomeres. Eventually, we demonstrated that Calstabin2 deletion resulted in AKT phosphorylation, augmented mTOR activity, and impaired autophagy in the heart. Taken together, our results identify Calstabin2 as a key modulator of cardiac aging and indicate that the activation of the AKT/mTOR pathway plays a mechanistic role in such a process.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.