Objectives: R) has emerged as a pivotal regulator of cardioprotective signaling. Currently, our aim is to elucidate the contribution of AA1R and AMPK-mediated autophagy in RIPC-induced cardioprotection. Materials and Methods: R antagonist) and BML-275 (AMPK inhibitor), respectively. Results: ), and other biochemical markers (increased TBARS, decreased GSH and catalase, increased TNF-α, TGF-β, Bax, and caspase-3). RIPC significantly attenuated these deleterious alterations, restoring both biochemical and functional parameters. However, the administration of DPCPX and BML-275 markedly abrogated the cardioprotective benefits conferred by RIPC. Conclusion: R and AMPK underscores an integrated adaptive mechanism that preserves myocardial integrity during IRI. This mechanistic insight provides a rationale for exploring AA1R-AMPK axis modulation as a therapeutic avenue for clinical cardioprotection.
Kumar et al. (2026) studied this question.