Review demonstrates Rolipram's potential to reduce inflammation and oxidative stress in ischemia-reperfusion injury, suggesting further clinical exploration.
Ischemia-reperfusion injury (IRI) remains a significant clinical challenge due to the complexity of its pathophysiology, which encompasses oxidative stress, inflammation, and regulated cell death. The evidence reviewed in this study highlights the promising role of Rolipram as a potential therapeutic agent for mitigating ischemia-reperfusion (I/R)-induced tissue damage. By increasing intracellular cAMP levels, Rolipram modulates key molecular pathways, including NF-κB, MAPK, and CREB, leading to a reduction in pro-inflammatory cytokine production, an inhibition of oxidative stress, and an enhancement of cellular survival mechanisms. Future research should aim to address these limitations through the use of advanced delivery systems, isoform-selective inhibitors, and well-controlled clinical trials. Nevertheless, the current evidence base supports the ongoing investigation of Rolipram as a multifunctional therapeutic candidate with the potential to significantly improve outcomes in ischemia-reperfusion injury. Article visualizations:
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Mammadov et al. (2025) studied this question.
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