RESOLUTION PHARMACOLOGY IN CHRONIC KIDNEY DISEASE: ROLE OF LIPID MEDIATORS IN TISSUE REPAIR

About 10-15% of people worldwide are affected by chronic kidney disease (CKD), a progressive disorder that causes chronic inflammation, oxidative stress, tubular injury, and fibrosis. RAAS inhibitors and sglt2 inhibitor drugs slow down disease progression but don't actively promote tissue regeneration. Why? In contrast, resolution pharmacology presents another therapeutic option where endogenous mechanisms that resolve inflammation and restore tissue homeostasis are enhanced to improve healing. Lipoxins, resolving and lipid mediators (masins) are examples of bioactive fatty acid molecules that act as "pro-resolution mediator"(spm), suppressing inflammation, increasing efferocytosis, decreasing fibrositis, and encouraging renal repair. Preclinical studies reveal that spms decrease renal inflammation, prevent kidney damage, and minimize fibrotic development in many models of CKD. The review summarizes the biosynthesis, receptor pharmacology, and nephroprotective mechanisms of spms, as well as the current translational obstacles and future opportunities.[1,4,20,27]