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Glomerular Mesangial Proliferation is Mitigated by sEH/COX‐2 Dual‐Inhibition

Chronic kidney disease afflicts millions across the globe, with focal segmental glomerulosclerosis (FSGS) being the most prevalent type of renal disorder. FSGS can result in irreparable damage to the kidney, and even death, if untreated. The kidney filters blood via a network of highly vascularized modules called glomeruli, of which each kidney has approximately one million, and those afflicted with FSGS exhibit damage to these filters. Intraglomerular capillaries are supported by a matrix of cells called the mesangium, and it believed that signals triggering mesangial hypertrophy and proliferation may exacerbate damage to the glomerulus in those with FSGS. Epoxyeicosatrienoic acids (EETs) are positive mediators of renal health and function. Conversely, some EET metabolites are intimated to stimulate mesangial proliferation, which is known to damage the glomerulus. EETs are most notably metabolized by soluble epoxide hydrolase (sEH), but they can also be modified by other enzymes such as cyclooxygenase‐2 (COX‐2), and we have developed a novel drug, PTUPB, that serves as a dual sEH/COX‐2 inhibitor. The objective of this research is to determine if either our non‐hydrolyzable 8,9‐EET analog, or PTUPB, reduces angiotensin II‐associated mesangial proliferation by decreasing the formation of potentially deleterious EET metabolites. Our long term goal is to mitigate the damage caused by FSGS through a better understanding of the role of EETs and their metabolites in glomerular function.