PGC-1α protects from myocardial ischaemia-reperfusion injury by regulating mitonuclear communication.
Yan-Qing LiYan JiaoYa-Nan LiuJia-Ying FuLian-Kun SunJing SuPublished in: Journal of cellular and molecular medicine (2021)
The recovery of blood supply after a period of myocardial ischaemia does not restore the heart function and instead results in a serious dysfunction called myocardial ischaemia-reperfusion injury (IRI), which involves several complex pathophysiological processes. Mitochondria have a wide range of functions in maintaining the cellular energy supply, cell signalling and programmed cell death. When mitochondrial function is insufficient or disordered, it may have adverse effects on myocardial ischaemia-reperfusion and therefore mitochondrial dysfunction caused by oxidative stress a core molecular mechanism of IRI. Peroxisome proliferator-activated receptor gamma co-activator 1α (PGC-1α) is an important antioxidant molecule found in mitochondria. However, its role in IRI has not yet been systematically summarized. In this review, we speculate the role of PGC-1α as a key regulator of mitonuclear communication, which may interacts with nuclear factor, erythroid 2 like -1 and -2 (NRF-1/2) to inhibit mitochondrial oxidative stress, promote the clearance of damaged mitochondria, enhance mitochondrial biogenesis, and reduce the burden of IRI.
Keyphrases
- oxidative stress
- nuclear factor
- left ventricular
- acute myocardial infarction
- skeletal muscle
- cerebral ischemia
- diabetic rats
- dna damage
- ischemia reperfusion injury
- cell death
- induced apoptosis
- toll like receptor
- acute ischemic stroke
- reactive oxygen species
- endoplasmic reticulum
- heart failure
- transcription factor
- single cell
- cell therapy
- signaling pathway
- inflammatory response
- immune response
- blood brain barrier
- emergency department
- risk factors
- adverse drug
- anti inflammatory