ArticlePloS one2013
Disruption of calcium homeostasis in cardiomyocytes underlies cardiac structural and functional changes in severe sepsis.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 2 of them syntheses that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
32 citing papers in PubMed, 2 syntheses or guidelines pooled it, 69 citations in OpenAlex.
- MicroRNAs as regulators of cardiac dysfunction in sepsis: pathogenesis and diagnostic potential.Frontiers in cardiovascular medicine · 2025Pooled it
- The Value of Decreased Thyroid Hormone for Predicting Mortality in Adult Septic Patients: A Systematic Review and Meta-Analysis.Scientific reports · 2018Pooled it
- Sepsis-Induced Cardiomyopathy and Cardiac Arrhythmias: Pathophysiology and Implications for Novel Therapeutic Approaches.Biomedicines · 2025Review
- PLK2 and the GSK3β-NRF2 Axis: A Promising Therapeutic Target for Sepsis-Induced Cardiac Injury?American journal of hypertension · 2025Article
- 5-Hydroxymethylcytosine signatures as diagnostic biomarkers for septic cardiomyopathy.Scientific reports · 2025Article
- Acute Kidney Injury During Sepsis and Prognostic Role of Coexistent Chronic Heart Failure.Journal of clinical medicine · 2025Review
- Myocardial calcification: case reports and a systematic review.European heart journal. Imaging methods and practice · 2024Article
- Exploring the Risk Factors and Possible Role of Calcium in Infective Endocarditis.Diagnostics (Basel, Switzerland) · 2023Review
- Molecular explanation of Wnt/βcatenin antagonist pyrvinium mediated calcium equilibrium changes in aging cardiovascular disorders.Molecular biology reports · 2022Review
- Modulation of the mTOR Pathway by Curcumin in the Heart of Septic Mice.Pharmaceutics · 2022Article
- Review
- Calpains as Potential Therapeutic Targets for Myocardial Hypertrophy.International journal of molecular sciences · 2022Review
- Inhibition of the NLRP3/IL-1β axis protects against sepsis-induced cardiomyopathy.Journal of cachexia, sarcopenia and muscle · 2021Article
- Transcriptome and Literature Mining Highlight the Differential Expression of ERLIN1 in Immune Cells during Sepsis.Biology · 2021Article
- Wnt/β-Catenin Antagonist Pyrvinium Exerts Cardioprotective Effects in Polymicrobial Sepsis Model by Attenuating Calcium Dyshomeostasis and Mitochondrial Dysfunction.Cardiovascular toxicology · 2021Article
- Dantrolene repurposed to treat sepsis or septic shock and COVID-19 patients.European review for medical and pharmacological sciences · 2021Review
- Article
- Breakdown of Filamentous Myofibrils by the UPS-Step by Step.Biomolecules · 2021Review
- Effect of Verapamil, an L-Type Calcium Channel Inhibitor, on Caveolin-3 Expression in Septic Mouse Hearts.Oxidative medicine and cellular longevity · 2021Article
- Heart Slices to Model Cardiac Physiology.Frontiers in pharmacology · 2021Review
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 2 countries.
Funding
Abstract
Sepsis, a major cause of morbidity/mortality in intensive care units worldwide, is commonly associated with cardiac dysfunction, which worsens the prognosis dramatically for patients. Although in recent years the concept of septic cardiomyopathy has evolved, the importance of myocardial structural alterations in sepsis has not been fully explored. This study offers novel and mechanistic data to clarify subcellular events that occur in the pathogenesis of septic cardiomyopathy and myocardial dysfunction in severe sepsis. Cultured neonatal mice cardiomyocytes subjected to serum obtained from mice with severe sepsis presented striking increment of [Ca(2+)]i and calpain-1 levels associated with decreased expression of dystrophin and disruption and derangement of F-actin filaments and cytoplasmic bleb formation. Severe sepsis induced in mice led to an increased expression of calpain-1 in cardiomyocytes. Moreover, decreased myocardial amounts of dystrophin, sarcomeric actin, and myosin heavy chain were observed in septic hearts associated with depressed cardiac contractile dysfunction and a very low survival rate. Actin and myosin from the sarcomere are first disassembled by calpain and then ubiquitinated and degraded by proteasome or sequestered inside specialized vacuoles called autophagosomes, delivered to the lysosome for degradation forming autophagolysosomes. Verapamil and dantrolene prevented the increase of calpain-1 levels and preserved dystrophin, actin, and myosin loss/reduction as well cardiac contractile dysfunction associated with strikingly improved survival rate. These abnormal parameters emerge as therapeutic targets, which modulation may provide beneficial effects on future vascular outcomes and mortality in sepsis. Further studies are needed to shed light on this mechanism, mainly regarding specific calpain inhibitors.
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Registered trials
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