Editorial on sartans and skeletal muscle regeneration: rethinking fibrosis as a modifiable target in traumatic injury.

Abstract

Traumatic muscle injuries are common yet often lead to incomplete recovery, despite the high regenerative potential of skeletal muscle. A major obstacle is fibrosis, which replaces functional tissue with disorganised extracellular matrix, impairing contractility and healing. Central to this maladaptive response is the TGF-β1 pathway, a conserved fibrogenic signal also implicated in cardiac, hepatic, and renal fibrosis. This has prompted interest in repurposing antifibrotic agents, particularly angiotensin II receptor blockers (ARBs), or sartans. These drugs, widely used for hypertension, inhibit TGF-β1 activation via AT1R antagonism. Preclinical studies in murine models have shown that sartans reduce collagen deposition, promote muscle regeneration, and improve functional outcomes after injury. Some also activate additional regenerative pathways, such as PPAR-γ. Although no clinical trials have evaluated ARBs for muscle injuries, preliminary data from orthopaedic settings suggest potential benefits. Given their safety, availability, and biological plausibility, sartans represent a promising avenue for therapeutic modulation of fibrosis in muscle trauma. Future research should clarify optimal timing, dosing, and patient selection to translate these findings into clinical practice.