MFN2: Shaping mitochondria and cardiac adaptations to hypoxia
Author:
Affiliation:
1. Department of Sport Science University of Innsbruck Innsbruck Austria
2. Institute of Sport Sciences University of Lausanne Lausanne Switzerland
Publisher
Wiley
Subject
Physiology
Link
https://onlinelibrary.wiley.com/doi/pdf/10.1111/apha.14026
Reference7 articles.
1. MFN2 deficiency promotes cardiac response to hypobaric hypoxia by reprogramming cardiomyocyte metabolism
2. Mitochondrial quality surveillance as a therapeutic target in myocardial infarction
3. Hypoxia-reprogramed megamitochondrion contacts and engulfs lysosome to mediate mitochondrial self-digestion
4. Dynamin-Related Protein 1–Mediated Mitochondrial Mitotic Fission Permits Hyperproliferation of Vascular Smooth Muscle Cells and Offers a Novel Therapeutic Target in Pulmonary Hypertension
5. MFN2-mediated mitochondrial fusion facilitates acute hypobaric hypoxia-induced cardiac dysfunction by increasing glucose catabolism and ROS production
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