The heart oxidizes fatty acids for its energy production. The physiological balance between fatty acid uptake and its oxidation prevents lipid accumulation in cardiac myocytes. However, accumulation of lipids due to various processes such as obesity, diabetes, heart failure, myocardial ischemia or infarction can result in damage to the heart tissue, also known as cardiolipotoxicity. We present a unique case of a 69-year-old gentleman with a history of heart failure and ventricular tachycardia. Endomyocardial biopsy to assess for restrictive cardiomyopathy/amyloid showed no evidence of amyloid, significant inflammation or fibrosis, but did show intracellular accumulation of significant amorphous material in most cardiac myocytes. We review the literature regarding the pathogenesis of cardiolipotoxicity, which has no definite cause or treatment yet identified.
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http://dx.doi.org/10.2217/fca-2020-0076 | DOI Listing |
Chaos
January 2025
School of Physics and Information Technology, Shaanxi Normal University, Xi'an 710062, China.
Arrhythmia of the heart is a dangerous and potentially fatal condition. The current widely used treatment is the implantable cardioverter defibrillator (ICD), but it is invasive and affects the patient's quality of life. The sonogenetic mechanism proposed here focuses ultrasound on a cardiac tissue, controls endogenous stretch-activated Piezo1 ion channels on the focal region's cardiomyocyte sarcolemma, and restores normal heart rhythm.
View Article and Find Full Text PDFCurr Cardiol Rep
January 2025
Department of Zoology, Trivenidevi Bhalotia College (Affiliated to Kazi Nazrul University), College Para Rd, Raniganj, 713347, West Bengal, India.
Purpose Of Review: This review investigates how post-injury cellular signaling and energy metabolism are two pivotal points in zebrafish's cardiomyocyte cell cycle re-entry and proliferation. It seeks to highlight the probable mechanism of action in proliferative cardiomyocytes compared to mammals and identify gaps in the current understanding of metabolic regulation of cardiac regeneration.
Recent Findings: Metabolic substrate changes after birth correlate with reduced cardiomyocyte proliferation in mammals.
J Exp Biol
January 2025
Hannover Medical School, Institute of Functional and Applied Anatomy, 30625 Hanover, Germany.
Small mammals have a higher heart rate and, relative to body mass (Mb), a higher metabolic rate than large mammals. In contrast, heart weight and stroke volume scale linearly with Mb. With mitochondria filling approximately 50% of a shrew cardiomyocyte - space unavailable for myofibrils - it is unclear how small mammals generate enough contractile force to pump blood into circulation.
View Article and Find Full Text PDFCirc Res
January 2025
Department of Physiology, Institute of Functional Genomics and Research Institute of Medical Science, Konkuk University School of Medicine, Chungju, Republic of Korea (H.L., S.P., J.R.A., M.S.S., H.J.N., B.K., Y.M.B.).
Orphanet J Rare Dis
January 2025
Department of Cardiac Physiology, National Cerebral and Cardiovascular Center Research Institute, 6-1 Kishibe-Shimmachi, Suita, Osaka, 564-8565, Japan.
Background: Transient receptor potential cation channel subfamily V member 2 (TRPV2) functions as a stretch-sensitive calcium channel, with overexpression in the sarcolemma of skeletal and cardiac myocytes leading to detrimental calcium influx and triggering muscle degeneration. In our previous pilot study, we showed that tranilast, a TRPV2 inhibitor, reduced brain natriuretic peptide levels in two patients with muscular dystrophy and advanced heart failure. Building on this, we performed a single-arm, open-label, multicenter study herein to evaluate the safety and efficacy of tranilast in the treatment of advanced heart failure in patients with muscular dystrophy.
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