The ultrastructure of myocardial cells of the left, right ventricle, and the ventricular septum was studied in the Altai and Pamir Yaks permanently living at the altitude of 3000-3600 m. Electron microscopic studies of myocardial cells revealed, along with the normal mitochondria, the ones with a peculiar structure of the cristae; these had the appearance of polyhedral wavy membranes in some groups of the mitochondria, and of polyhedral netted structures - in the others. Considerable accumulations of glycogen granules were found beneath the sarcolemma, in the perinuclear cytoplasmic zone and between the myofibrils. The results suggest that by undulating and creating a certain structural regularity the mitochondrial cristae increased their active area ensuring the efficacy of the mitochondrial function. Considerable accumulation of glycogen granules in the majority of myocardial cells seems to maintain the energy potential of the myocardium preventing the development of hypoxia.
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Sci Rep
January 2025
Shaoxing Maternity and Child Health Care Hospital, No. 222 Fenglin East Road, Shaoxing, 312000, Zhejiang, China.
Pediatric non-alcoholic fatty liver disease (NAFLD) is emerging as a worldwide health concern with the potential to advance to cirrhosis and liver cancer. NAFLD can also directly contribute to heart problems through inflammation and insulin resistance, even in individuals without other risk factors. The pathological mechanisms of NAFLD are linked to functional differences of miRNAs in different biological environments.
View Article and Find Full Text PDFNat Commun
January 2025
Smidt Heart Institute, Cedars-Sinai Medical Center, Los Angeles, California, CA, USA.
Myocardial fibrosis leads to cardiac dysfunction and arrhythmias in heart failure with preserved ejection fraction (HFpEF), but the underlying mechanisms remain poorly understood. Here, RNA sequencing identifies Forkhead Box1 (FoxO1) signaling as abnormal in male HFpEF hearts. Genetic suppression of FoxO1 alters the intercellular communication between cardiomyocytes and fibroblasts, alleviates abnormal diastolic relaxation, and reduces arrhythmias.
View Article and Find Full Text PDFPLoS One
January 2025
Department of Pathology, 906 Hospital of Joint Logistic Support Force of PLA, Ningbo, Zhejiang, China.
Objective: To investigate the effects and mechanisms of miRNA 221 on myocardial ischemia/reperfusion injury (MIRI) in mice through the regulation of phospholamban (PLB) expression.
Methods: The MIRI mouse model was created and mice were divided into sham, MIRI, MIRI+ 221, and MIRI+ scr groups, with miRNA 221 overexpression induced in the myocardium of MIRI mice by targeted myocardial injection. Quantitative RT-PCR analysis was performed to observe the variation in miRNA 221, PLB, SERCA2, RYR2, NCX1, Cyt C and caspase 3 mRNA levels in myocardium, while Western blot assessed the levels of PLB, p-PLB (Ser16), p-PLB (Thr17), SERCA2, RYR2, NCX1, Cyt C and caspase 3 proteins.
Metabol Open
March 2025
Department of Biochemistry and Microbiology, University of Zululand, KwaDlangezwa, 3886, South Africa.
Dyslipidemia is a prominent pathological feature responsible for oxidative stress-induced cardiac damage. Due to their high antioxidant content, dietary compounds, such as aspalathin and sulforaphane, are increasingly explored for their cardioprotective effects against lipid-induced toxicity. Cultured H9c2 cardiomyoblasts, an in vitro model routinely used to assess the pharmacological effect of drugs, were pretreated with the dietary compounds, aspalathin (1 μM) and sulforaphane (10 μM) before exposure to palmitic acid (0.
View Article and Find Full Text PDFMol Med
January 2025
The First People's Hospital of Lin'an District, No. 360, Yikang Street, Jinnan Subdistrict, Lin'an District, Hangzhou, Zhejiang, 311300, China.
Background: Myocardial infarction (MI) remains a leading cause of mortality globally, often resulting in irreversible damage to cardiomyocytes. Ferroptosis, a recently identified form of regulated cell death driven by iron-dependent lipid peroxidation, has emerged as a significant contributor to post-MI cardiac injury. The endoplasmic reticulum (ER) stress response has been implicated in exacerbating ferroptosis.
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