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Multi-omics map revealed PPARalpha activation protecting against myocardial ischemia-reperfusion injury by maintaining cardiac metabolic homeostasis

Gao, Y.; Huang, F.; Ruan, F.; Lai, D.; Zhang, Z.; Zhang, Y.; Zhu, J.; Lu, Y.; Shen, L.; He, J.; Liu, Y.; Fu, G.; Zhu, Y.; Shen, L.; Zhuang, L.

2023-08-19 cell biology
10.1101/2023.08.17.551936 bioRxiv
Show abstract

Timely percutaneous coronary intervention is the most effective initial therapy for the acute myocardial infarction (MI). However, the mechanism in energy metabolism underlying time-dependent coronary reperfusion remains largely unknown. Here, we generated an integrative map of cardiac cells using bulk and single-nucleus RNA-seq combined with metabolomics profiling of hearts with reperfusion at distinct time points post MI in rat. We found early time reperfusion (ETR), but not late time reperfusion (LTR) reduced myocardial injury by maintaining cardiac energy homeostasis. PPAR was identified as a key regulator for maintaining fatty acid metabolism after MI/R injury. Importantly, pretreatment with FDA-approved PPAR agonist, fenofibrate, improved the transcriptional signatures, and ameliorated the function of the MI/R injured hearts, particularly in the ETR. Together, our data not only deciphered the protective effect of ETR by maintaining cardiac energy homeostasis, but also provided insights into the translational potential of PPAR activation in alleviating MI/R injury.

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"Similar papers" are the closest papers from that journal in the model's embedding space. They show what the match is built on, but the ranking comes mostly from a classifier over the whole training set, not from these examples alone.