The Impact of Telmisartan on Inflammation and Oxidative Stress in Human Studies and Murine Models: A Narrative Review

Abstract

Chronic inflammation and oxidative stress play a critical role in conditions such as atherosclerosis, metabolic syndrome, and diabetic nephropathy. Telmisartan is a unique long-acting ARB due to its dual mechanism of action. In addition to blocking the AT1R, it acts as a partial agonist for peroxisome proliferator-activated receptor-gamma (PPAR-γ). It is also characterized by high lipophilicity compared to other drugs in its class, facilitating tissue penetration into the central nervous system. The objective of this narrative review is to bridge the gap between murine models of oxidative stress and inflammation and human clinical outcomes across the cardiovascular, renal, hepatic, neurological, and autoimmune systems. Across extensive human clinical trials and murine models, telmisartan demonstrates unique potential as a multi-system anti-inflammatory and antioxidant agent that actively suppresses pro-apoptotic and fibrotic cascades. Beyond these systemic effects, telmisartan confers localized vascular benefits by actively stabilizing coronary plaques and suppressing cardiac inflammation. While its cardiovascular and renal benefits are the most widely investigated, it also demonstrates profound extra-cardiac efficacy. In particular, telmisartan improves neuroinflammation in neurodegenerative diseases, metabolic profiles in hepatic steatosis, and protects against gastrointestinal and musculoskeletal inflammation. But its protective effects are limited for established HIV fibrosis and severe primary autoimmune conditions like psoriasis. In conclusion, telmisartan is a cardiometabolic and immunomodulatory drug, extending the clinical use beyond hypertension.