The Effect of Metformin on Inflammatory and Fibrotic Responses in Renal Fibrosis
Abstract
Chronic kidney disease (CKD) is a worldwide public health problem, with adverse outcomes of kidney failure, cardiovascular disease, and premature death. It is well recognised that renal fibrosis is the unifying pathology in almost all forms of progressive CKD. To date, kidney transplantation and dialysis are the only options for the management of end-stage kidney disease, which results in a significant burden on the health system. Hence innovative strategies are needed to both prevent and treat CKD. It is well recognised that inflammatory pathways play a central role in the progression of CKD and TGFβ-1 is a profibrotic cytokine found in CKD regardless of aetiology, which initiates and modulates a variety of pathophysiological processes. In renal disease, TGFβ-1 is upregulated and induces renal cells to produce extracellular matrix proteins leading to glomerulosclerosis as well as tubulointerstitial fibrosis. Different types of renal cells undergo different pathophysiological changes induced by TGF-β1, leading to apoptosis, hypertrophy and abnormalities of podocyte foot processes, which ultimately result in renal dysfunction. Regardless of the cause of CKD, multiple cytokines, growth factors, pro-inflammatory and fibrotic signalling pathways participate in the development of the pathological process in the kidney. Excessive deposition of extracellular matrix (ECM) is the most striking and common feature of renal fibrosis. Hence, targeting inflammatory and fibrotic responses,…
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