ArticleInternational journal of general medicine2026
GPR55 Inhibits Inflammatory Factor TNF-α-Mediated RhoA/ROCK2/IκBα/p65 Signaling Pathway to Alleviate Diabetic Cardiomyopathy in Rats.
Article in International journal of general medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Challenges remain to the pathogenesis and targeted intervention of diabetic cardiomyopathy (DCM). G protein-coupled receptor 55 (GPR55) plays an important role in the onset and progression of DCM, however, the regulatory mechanism remains unknown. Methods: In this study, we successfully induced DCM in rats by intraperitoneal injection of streptozotocin and explored the efficacy of GPR55 in ameliorating DCM through the intervention of GPR55 activator O-1602. Results: The results showed that the intervention of O-1602 alleviated pathological lesions in cardiac tissues of DCM rats, reduced blood glucose levels, inhibited oxidative stress and suppressed inflammatory pathways. In addition, in vitro H9C2 cell assay confirmed the ameliorative effect of O-1602. The mechanism of DCM alleviation by GPR55 revealed the contribution of the inhibited RhoA/ROCK2/IκBα/p65 signaling pathway. Conclusion: Therefore, it is speculated that GPR55 alleviates DCM by inhibiting the TNF-α-mediated RhoA/ROCK2/IκBα/p65 signaling pathway, which highlights the potential role of GPR55 in the treatment of DCM, and provides basic data to support future studies.
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