Chronic kidney disease (CKD) is a progressive, irreversible condition characterized by reduced kidney function, tubular injury, oxidative stress, and inflammation. It is a leading global health burden, often asymptomatic in early stages but leading to kidney failure. CKD is caused by dysregulated signaling pathways that promote fibrosis, with TGF-β playing a central role in promoting transdifferentiation of renal tubular epithelial cells into mesenchymal cells, leading to irreversible kidney injury. Current therapies aim to delay progression, but new antifibrotic agents targeting TGF-β signaling are being explored. Imaging techniques like diffusion-weighted MRI and shear wave elastography are less invasive for fibrosis staging. Kidney biopsy is the gold standard for diagnosis, but it has limitations due to sampling bias and invasiveness. Biomarkers such as TGF-β1 and CTGF are being studied for their role in fibrosis. Fibrosis in CKD involves excessive extracellular matrix accumulation, leading to structural damage and irreversible injury. The fibrotic niche includes various cell types and extracellular components that promote fibroblast activation and ECM deposition. TGF-β signaling is a key driver of fibrosis, with its inhibition being a promising therapeutic approach. Antifibrotic drugs like pirfenidone are in clinical trials. Other approaches include targeting microRNA-21 and exploring novel therapies such as stem cell-based treatments. Future treatments may focus on TGF-β signaling, ECM proteins, and other pathways involved in fibrosis. SGLT2 inhibitors show promise in reducing fibrosis and improving renal outcomes. Clinical trials are ongoing to evaluate the efficacy of these therapies in CKD.Chronic kidney disease (CKD) is a progressive, irreversible condition characterized by reduced kidney function, tubular injury, oxidative stress, and inflammation. It is a leading global health burden, often asymptomatic in early stages but leading to kidney failure. CKD is caused by dysregulated signaling pathways that promote fibrosis, with TGF-β playing a central role in promoting transdifferentiation of renal tubular epithelial cells into mesenchymal cells, leading to irreversible kidney injury. Current therapies aim to delay progression, but new antifibrotic agents targeting TGF-β signaling are being explored. Imaging techniques like diffusion-weighted MRI and shear wave elastography are less invasive for fibrosis staging. Kidney biopsy is the gold standard for diagnosis, but it has limitations due to sampling bias and invasiveness. Biomarkers such as TGF-β1 and CTGF are being studied for their role in fibrosis. Fibrosis in CKD involves excessive extracellular matrix accumulation, leading to structural damage and irreversible injury. The fibrotic niche includes various cell types and extracellular components that promote fibroblast activation and ECM deposition. TGF-β signaling is a key driver of fibrosis, with its inhibition being a promising therapeutic approach. Antifibrotic drugs like pirfenidone are in clinical trials. Other approaches include targeting microRNA-21 and exploring novel therapies such as stem cell-based treatments. Future treatments may focus on TGF-β signaling, ECM proteins, and other pathways involved in fibrosis. SGLT2 inhibitors show promise in reducing fibrosis and improving renal outcomes. Clinical trials are ongoing to evaluate the efficacy of these therapies in CKD.