ArticleAmerican journal of physiology. Heart and circulatory physiology2017
Desmin loss and mitochondrial damage precede left ventricular systolic failure in volume overload heart failure.
Article in American journal of physiology. Heart and circulatory physiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.
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Who cites it
23 citing papers in PubMed, 1 synthesis or guideline pooled it, 43 citations in OpenAlex.
- Guidelines for authors and reviewers on antibody use in physiology studies.American journal of physiology. Heart and circulatory physiology · 2018Guideline
- Mechanisms of protein degradation in atrophying muscles: What have we learned during the past decade?The Journal of biological chemistry · 2026Review
- The Role of Mitophagy in Cardiac Metabolic Remodeling of Heart Failure: Insights of Molecular Mechanisms and Therapeutic Prospects.Journal of cardiovascular translational research · 2025Review
- The deubiquitinase USP5 prevents accumulation of protein aggregates in cardiomyocytes.Science advances · 2025Article
- Adapting cytoskeleton-mitochondria patterning with myocyte differentiation by promyogenic PRR33.Cell death and differentiation · 2025Article
- Type III intermediate filaments in redox interplay: key role of the conserved cysteine residue.Biochemical Society transactions · 2024Review
- Improved mitochondrial function in the hearts of sarcolipin-deficient dystrophin and utrophin double-knockout mice.JCI insight · 2024Article
- Critical contribution of mitochondria in the development of cardiomyopathy linked to desmin mutation.Stem cell research & therapy · 2024Article
- Remodeling of Cardiomyocytes: Study of Morphological Cellular Changes Preceding Symptomatic Ischemic Heart Failure.International journal of molecular sciences · 2023Article
- Desmin Reorganization by Stimuli Inducing Oxidative Stress and Electrophiles: Role of Its Single Cysteine Residue.Antioxidants (Basel, Switzerland) · 2023Article
- Pimobendan prevents cardiac dysfunction, mitigates cardiac mitochondrial dysfunction, and preserves myocyte ultrastructure in a rat model of mitral regurgitation.BMC veterinary research · 2023Article
- Mitochondrial dysfunction in human hypertrophic cardiomyopathy is linked to cardiomyocyte architecture disruption and corrected by improving NADH-driven mitochondrial respiration.European heart journal · 2023Article
- Mitochondrial haplotype modulates genome expression and mitochondrial structure/function in cardiomyocytes following volume overload.American journal of physiology. Heart and circulatory physiology · 2023Article
- Desmin aggrephagy in rat and human ischemic heart failure through PKCζ and GSK3β as upstream signaling pathways.Cell death discovery · 2021Article
- Desmin Correlated with Cx43 May Facilitate Intercellular Electrical Coupling during Chronic Heart Failure.Evidence-based complementary and alternative medicine : eCAM · 2021Article
- Chronic cardiac structural damage, diastolic and systolic dysfunction following acute myocardial injury due to bromine exposure in rats.Archives of toxicology · 2021Article
- Review
- Cardiac remodeling secondary to chronic volume overload is attenuated by a novel MMP9/2 blocking antibody.PloS one · 2020Article
- Cardiac Tissue Chips (CTCs) for Modeling Cardiovascular Disease.IEEE transactions on bio-medical engineering · 2019Article
- Contribution of DNA methylation in chronic stress-induced cardiac remodeling and arrhythmias in mice.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019Article
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
Heart failure due to chronic volume overload (VO) in rats and humans is characterized by disorganization of the cardiomyocyte desmin/mitochondrial network. Here, we tested the hypothesis that desmin breakdown is an early and continuous process throughout VO. Male Sprague-Dawley rats had aortocaval fistula (ACF) or sham surgery and were examined 24 h and 4 and 12 wk later. Desmin/mitochondrial ultrastructure was examined by transmission electron microscopy (TEM) and immunohistochemistry (IHC). Protein and kinome analysis were performed in isolated cardiomyocytes, and desmin cleavage was assessed by mass spectrometry in left ventricular (LV) tissue. Echocardiography demonstrated a 40% decrease in the LV mass-to-volume ratio with spherical remodeling at 4 wk with ACF and LV systolic dysfunction at 12 wk. Starting at 24 h and continuing to 4 and 12 wk, with ACF there is TEM evidence of extensive mitochondrial clustering, IHC evidence of disorganization associated with desmin breakdown, and desmin protein cleavage verified by Western blot analysis and mass spectrometry. IHC results revealed that ACF cardiomyocytes at 4 and 12 wk had perinuclear translocation of αB-crystallin from the Z disk with increased α, β-unsaturated aldehyde 4-hydroxynonelal. Use of protein markers with verification by TUNEL staining and kinome analysis revealed an absence of cardiomyocyte apoptosis at 4 and 12 wk of ACF. Significant increases in protein indicators of mitophagy were countered by a sixfold increase in p62/sequestosome-1, which is indicative of an inability to complete autophagy. An early and continuous disruption of the desmin/mitochondrial architecture, accompanied by oxidative stress and inhibition of apoptosis and mitophagy, suggests its causal role in LV dilatation and systolic dysfunction in VO.
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