Key result
Hypoxia promoted TGF-β-induced collagen deposition and myocardial fibrosis by inducing endoplasmic reticulum stress and oxidative stress in HL-1 cardiomyocytes, which was effectively alleviated by the antioxidant N-Acetylcysteine.
Why the study?
Hypoxia is known to induce myocardial hypoxia, but the underlying mechanisms remain unclear.
Hypoxia induces myocardial fibrosis via endoplasmic reticulum and oxidative stress, suggesting antioxidant therapy as a potential treatment strategy.
Hypoxia-driven fibrosis via ER/oxidative stress is hypothesis-generating; leaves open in vivo relevance and therapeutic targeting.
SUMMARY Myocardial cells, fibroblasts and vascular cells in the heart are connected by a complex matrix mainly composed of fibrillar collagen, which helps to protect the integrity and compliance of the heart structure. Previous studies have shown that hypoxia can induce myocardial hypoxia, but the mechanism is still unclear. In this study, we found that hypoxia promotes TGF beta induced collagen deposition and myocardial fibrosis by inducing Endoplasmic reticulum stress and oxidative stress in cardiomyocytes. Moreover, we also found that antioxidant drugs can effectively alleviate hypoxia induced myocardial fibrosis. Therefore, our study provides an experimental basis for the treatment of myocardial fibrosis.
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Jiang et al. (2023) studied Myocardial fibrosis. Hypoxia and N-Acetylcysteine (NAC) vs. Normoxia / Control cells was evaluated on Expression of fibrosis markers (collagen I, α-SMA) and ER stress markers (GRP78, CHOP). Hypoxia promoted TGF-β-induced collagen deposition and myocardial fibrosis by inducing endoplasmic reticulum stress and oxidative stress in HL-1 cardiomyocytes, which was effectively alleviated by the antioxidant N-Acetylcysteine.
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