Fibrosis, characterised by the excessive deposition of extracellular matrix via activated fibroblasts, is a pathological feature of several chronic inflammatory disorders, which collectively contribute significantly to global morbidity and mortality. Despite this, current anti-fibrotic therapies are of limited efficacy. However, incretin-based therapies, primarily glucagon-like peptide-1 (GLP-1) receptor agonists, are now emerging as candidate drugs for modulating fibrotic signalling pathways. This review synthesises the growing body of preclinical and clinical evidence that incretin receptor agonists exert direct and indirect anti-fibrotic effects. We detail the molecular mechanisms and survey the promising data across hepatic, cardiac, renal, lung, and joint tissues, which underscore the potential for repurposing of this drug class as a therapeutic strategy for fibro-inflammatory conditions.
Today’s society has gradually entered an aging phase, and among the elderly population, the risk of chronic kidney disease (CKD) is significantly increased. Renal fibrosis is the key pathological mechanism for the development of chronic kidney disease to end-stage renal disease. With the increase in age, the phenomenon of glomerular sclerosis and interstitial fibrosis in aging kidneys gradually aggravates, and the glomerular filtration rate (GFR) decreases, further affecting renal function. Fibrosis not only accelerates the loss of renal function but also significantly increases the risk of cardiovascular disease, which seriously affects the quality of life and life expectancy of patients. This paper reviews the relevant literature and discusses the characteristics of an aging kidney and the diagnostic methods for renal fibrosis.
