Aldehyde dehydrogenase 2 has cardioprotective effects on myocardial ischaemia/reperfusion injury via suppressing mitophagy
Open accessAbstract
Mitophagy, a selective form of autophagy, is excessively activated in myocardial ischemia/reperfusion (I/R). The study investigated whether aldehyde dehydrogenase 2 (ALDH2) exerted its cardioprotective effect by regulating mitophagy. Myocardial infarct size and apoptosis after I/R in rats were ameliorated by Alda-1, an ALDH2 activator, and aggravated by ALDH2 inhibition. Both in I/R rats and hypoxia/reoxygenation H9C2 cells, ALDH2 activation suppressed phosphatase and tensin homolog-induced putative kinase 1 (PINK1)/Parkin expression, regulating mitophagy, by preventing 4-hydroxynonenal, reactive oxygen species and mitochondrial superoxide accumulation. Furthermore, the effect was enhanced by ALDH2 inhibition. Thus, ALDH2 may protect hearts against I/R injury by suppressing PINK1/Parkin-dependent mitophagy.
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Excessive mitochondrial fission aggravates cardiac I/R injury via alternating the balance of pro- and anti-survival factors.
“Excessive mitochondrial fission aggravates cardiac I/R injury via alternating the balance of pro- and anti-survival factors [184].”
From AMPK, Mitochondrial Function, and Cardiovascular Disease (2020) · cites this paper as [184]
Mitochondrial homeostasis is a critical regulator of cell death during cardiac I/R injury, especially mitochondrial fission and mitophagy.
“Recently, mitochondrial homeostasis has been attributed as a critical regulator of cell death during cardiac I/R injury, especially mitochondrial fission and mitophagy [184].”
From AMPK, Mitochondrial Function, and Cardiovascular Disease (2020) · cites this paper as [184]
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- Authors
- Ji, W., Wei, S., Hao, P., Xing, J., Yuan, Q., Wang, J., Xu, F., & Chen, Y.
- Affiliations
- Shandong University (CN)
- Corresponding author
- Chen, Yuguo
- Venue
- Frontiers in Pharmacology
- Publisher
- Frontiers Media SA
- Published
- 2016-04-21
- Volume
- 7
- Pages
- 101-101
- ISSN
- 1663-9812 (ISSN-L)
- PMC
- PMC4838626
- OpenAlex
- W2336794657
- Cited by
- 106
- References
- 45
- Citations by year
- 2026: 7 · 2025: 11 · 2024: 8 · 2023: 18 · 2022: 9 · 2021: 9 · 2020: 18 · 2019: 7 · 2018: 9 · 2017: 8 · 2016: 2
- FWCI
- 7.86
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- cc-by
- Locations
- Frontiers in Pharmacology (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- Shandong University (2014QLKY04)
- Department of Science and Technology of Shandong Province (2014QLKY04)
- National Natural Science Foundation of China (81300103, 81300219, 81570401, 81571934, 81400284, 81400209, 81170136)
- Specialized Research Fund for the Doctoral Program of Higher Education of China (20130131110048)
- Topics
- Health Sciences › Medicine › Pathology and Forensic Medicine › Cardiac Ischemia and Reperfusion
- Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Aldose Reductase and Taurine
- Keywords
- ALDH2, cardioprotection, myocardial ischemia-reperfusion injury, mitophagy, PINK1/Parkin pathway, Alda-1, 4-hydroxynonenal, reactive oxygen species, mitochondrial superoxide, apoptosis, myocardial infarct size, hypoxia/reoxygenation
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