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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.

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Interleukin-34 (IL-34) was recently reported to be a new biomarker for atherosclerosis diseases, such as coronary artery disease and vascular dementia. IL-34 regulates the expression of proinflammatory cytokines (IL-17A, IL-1 and IL-6), which are classical cytokines involved in myocardial ischemia‒reperfusion (MI/R) injury. However, the exact role of IL-34 in MI/R remains unknown.

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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.

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Study Objective: Hypertrophic cardiomyopathy (HCM) is the most common genetic myocardial disorder increasingly characterized by concomitant metabolic syndrome. Cardiac rehabilitation (CR) has been shown to improve metabolic parameters in populations with heart failure and myocardial infarction. However, there is a paucity of data on the impact of CR in the HCM population with metabolic syndrome.

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Increased cardiac macrophages in -deficient hearts: revealing a potential role for macrophage in responding to embryonic myocardial abnormalities.

Front Genet

January 2025

Pediatric Translational Medicine Institute and Pediatric Congenital Heart Disease Institute, Shanghai Children's Medical Center, Shanghai Jiao Tong University School of Medicine, Shanghai, China.

Macrophages are known to support cardiac development and homeostasis, contributing to tissue remodeling and repair in the adult heart. However, it remains unclear whether embryonic macrophages also respond to abnormalities in the developing heart. Previously, we reported that the structural protein Sorbs2 promotes the development of the second heart field, with its deficiency resulting in atrial septal defects (ASD).

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