Mechanistic Insights into the Antihypertensive and Cardioprotective Actions of Corosolic Acid: A Narrative Review

Background: The specific mechanisms underlying the antihypertensive actions of corosolic acid (CA) have not been systematically elucidated. Methods: Evidence was categorized according to major signaling and physiological pathways, including the renin–angiotensin system (RAS), oxidative and inflammatory responses, endothelial and smooth muscle regulation (NO/cGMP and H2S/KATP), and kinase-mediated signaling (AMPK, NF-κB, JAK/STAT, PKC). Results: Consistent with in vitro and animal studies, CA has been reported to attenuate pro-hypertensive signaling through multiple pathways: (i) downregulating renin–angiotensin system-related cascades; (ii) reduction in reactive oxygen species and inflammatory mediators through activation of AMPK and inhibition of NF-κB and JAK/STAT pathways; (iii) improved vascular tone by enhancing NO/cGMP signaling, partly involving the H2S/KATP pathway, and inhibiting PKC. CA may indirectly contribute to blood pressure reduction by improving glucose and lipid metabolism and adipose tissue inflammation, thereby affecting metabolic risk factors. The existing evidence gaps include: lack of direct studies on voltage-gated, receptor-gated and store-regulated calcium channels; the specific effects on the isoforms of nitric oxide synthase (eNOS/iNOS/nNOS) and PKC are not known; limited human data on the antihypertensive efficacy, dose effect and safety of CA in humans are available. Conclusions: CA may have multi-targeted blood-pressure-lowering potential. Its clinical efficacy and safety require further confirmation.