ArticleBiochimica et biophysica acta2016
Disruption of calpain reduces lipotoxicity-induced cardiac injury by preventing endoplasmic reticulum stress.
Article in Biochimica et biophysica acta, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 56 citations in OpenAlex.
- JP2 and JCN Crosstalk Abrogate MURF1-Mediated JCN Ubiquitination and Degradation in Cardiomyocytes.JACC. Basic to translational science · 2026Article
- Comparative mathematical modeling reveals the differential effects of high-fat diet and ketogenic diet on the PI3K-Akt signaling pathway in heart.Nutrition & metabolism · 2024Article
- Possible role of endoplasmic reticulum stress in the pathogenesis of chronic adenoiditis and adenoid hypertrophy: A prospective, parallel-group study.Laryngoscope investigative otolaryngology · 2024Article
- Sustained over-expression of calpain-2 induces age-dependent dilated cardiomyopathy in mice through aberrant autophagy.Acta pharmacologica Sinica · 2022Article
- MLKL-mediated necroptosis is a target for cardiac protection in mouse models of type-1 diabetes.Cardiovascular diabetology · 2022Article
- The role of junctophilin proteins in cellular function.Physiological reviews · 2022Review
- Calpains as Potential Therapeutic Targets for Myocardial Hypertrophy.International journal of molecular sciences · 2022Review
- Gamma-Aminobutyrate Transaminase Protects against Lipid Overload-Triggered Cardiac Injury in Mice.International journal of molecular sciences · 2022Article
- Electroacupuncture pre-treatment alleviates sepsis-induced cardiac inflammation and dysfunction by inhibiting the calpain-2/STAT3 pathway.Frontiers in physiology · 2022Article
- The multifaceted roles of ER and Golgi in metabolic cardiomyopathy.Frontiers in cardiovascular medicine · 2022Review
- Integrative biology of extracellular vesicles in diabetes mellitus and diabetic complications.Theranostics · 2022Review
- Dapagliflozin Ameliorates STZ-Induced Cardiac Hypertrophy in Type 2 Diabetic Rats by Inhibiting the Calpain-1 Expression and Nuclear Transfer of NF-Computational and mathematical methods in medicine · 2022Article
- Therapeutic Approach of Flavonoid in Ameliorating Diabetic Cardiomyopathy by Targeting Mitochondrial-Induced Oxidative Stress.International journal of molecular sciences · 2021Review
- Cardiac-specific CGI-58 deficiency activates the ER stress pathway to promote heart failure in mice.Cell death & disease · 2021Article
- Ischemic stroke induces cardiac dysfunction and alters transcriptome profile in mice.BMC genomics · 2021Article
- Calpain-Mediated Mitochondrial Damage: An Emerging Mechanism Contributing to Cardiac Disease.Cells · 2021Review
- Therapeutic potential of targeting oxidative stress in diabetic cardiomyopathy.Free radical biology & medicine · 2021Review
- Effect of adenosine monophosphate-activated protein kinase-p53-Krüppel-like factor 2a pathway in hyperglycemia-induced cardiac remodeling in adult zebrafish.Journal of diabetes investigation · 2021Article
- Targeting JP2: A New Treatment for Pulmonary Hypertension.Oxidative medicine and cellular longevity · 2021Review
- Hydrogen sulfide regulates muscle RING finger-1 protein S-sulfhydration at CysBritish journal of pharmacology · 2020Article
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 3 countries.
Funding
Abstract
Diabetes and obesity are prevalent in westernized countries. In both conditions, excessive fatty acid uptake by cardiomyocytes induces cardiac lipotoxicity, an important mechanism contributing to diabetic cardiomyopathy. This study investigated the effect of calpain disruption on cardiac lipotoxicity. Cardiac-specific capns1 knockout mice and their wild-type littermates (male, age of 4weeks) were fed a high fat diet (HFD) or normal diet for 20weeks. HFD increased body weight, altered blood lipid profiles and impaired glucose tolerance comparably in both capns1 knockout mice and their wild-type littermates. Calpain activity, cardiomyocyte cross-sectional areas, collagen deposition and triglyceride were significantly increased in HFD-fed mouse hearts, and these were accompanied by myocardial dysfunction and up-regulation of hypertrophic and fibrotic collagen genes as well as pro-inflammatory cytokines. These effects of HFD were attenuated by disruption of calpain in capns1 knockout mice. Mechanistically, deletion of capns1 in HFD-fed mouse hearts and disruption of calpain with calpain inhibitor-III, silencing of capn1, or deletion of capns1 in palmitate-stimulated cardiomyocytes prevented endoplasmic reticulum stress, apoptosis, cleavage of caspase-12 and junctophilin-2, and pro-inflammatory cytokine expression. Pharmacological inhibition of endoplasmic reticulum stress diminished palmitate-induced apoptosis and pro-inflammatory cytokine expression in cardiomyocytes. In summary, disruption of calpain prevents lipotoxicity-induced apoptosis in cardiomyocytes and cardiac injury in mice fed a HFD. The role of calpain is mediated, at least partially, through endoplasmic reticulum stress. Thus, calpain/endoplasmic reticulum stress may represent a new mechanism and potential therapeutic targets for cardiac lipotoxicity.
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Registered trials
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.