AI Article Synopsis
- Diabetic cardiomyopathy (DCM) causes problems in heart cells by changing how mitochondria (the cell's energy factories) behave, leading to cell death and poor heart function.
- Researchers tested how changing these mitochondrial behaviors could help mice with DCM and found that blocking cell fission or encouraging cell fusion helped the heart work better.
- The treatments not only improved heart function but also reduced damage to heart cells and kept the mitochondria healthy, suggesting that fixing mitochondrial balance could lead to better heart health for people with similar problems.
Article Abstract
Diabetic cardiomyopathy (DCM) triggers a detrimental shift in mitochondrial dynamics, characterized by increased fission and decreased fusion, contributing to cardiomyocyte apoptosis and cardiac dysfunction. This study investigated the impact of modulating mitochondrial dynamics on DCM outcomes and underlying mechanisms in a mouse model. DCM induction led to upregulation of fission genes (Drp1, Mff, Fis1) and downregulation of fusion genes (Mfn1, Mfn2, Opa1). Inhibiting fission with Mdivi-1 or promoting fusion with Ginsenoside Rg1 preserved cardiac function, as evidenced by improved left ventricular ejection fraction (LVEF), fractional shortening (FS), and E/A ratio. Both treatments also reduced infarct size and attenuated cardiomyocyte apoptosis, indicated by decreased caspase-3 activity. Mechanistically, Mdivi-1 enhanced mitochondrial function by improving mitochondrial membrane potential, reducing reactive oxygen species (ROS) production, and increasing ATP generation. Ginsenoside Rg1 also preserved mitochondrial integrity and function under hypoxic conditions in HL-1 cardiomyocytes. These findings suggest that restoring the balance of mitochondrial dynamics through pharmacological interventions targeting either fission or fusion may offer a promising therapeutic strategy for mitigating MI-induced cardiac injury and improving patient outcomes.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11413890 | PMC |
| http://dx.doi.org/10.7150/ijms.98065 | DOI Listing |
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