Why the study?
Myocardial ischemia-reperfusion injury is an unresolved fatal complication in acute myocardial infarction, and the mechanisms by which GADD45G regulates it remain unclear.
SP1 promotes myocardial ischemia/reperfusion injury by transcriptionally upregulating GADD45G, identifying a potential therapeutic target for MIRI.
Identifies SP1-GADD45G axis as potential MIRI target; hypothesis-generating and should not yet change clinical practice.
Myocardial ischemia-reperfusion injury (MIRI) is an unresolved clinically fatal complication in the management of acute myocardial infarction (AMI). Growth arrest and DNA damage-inducible gene 45 Gamma (GADD45G) plays a vital role in the regulation of MIRI. However, the underlying mechanisms remain unclear. GADD45G and SP1 expression were upregulated in hypoxia/reoxygenation (H/R)-treated H9C2 cells. H/R treatment repressed H9C2 cell viability, and induced apoptosis, oxidative stress, and inflammatory response. Moreover, GADD45G deficiency could relieve H/R-triggered H9C2 cell injury. In mechanism, SP1 was a transcription factor of GADD45G and activated the transcription of GADD45G via binding to its promoter region. Besides, SP1 knockdown alleviated MI/R-induced pathological damage in the myocardial tissue of rats by regulating GADD45G. In conclusion, SP1 could promote H/R-induced cardiomyocyte injury and MI/R-caused rat myocardial tissue pathological injury by increasing GADD45G, providing a promising therapeutic target for MIRI treatment.
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Wang et al. (2026) studied this question.
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