2019 Volume 95 Issue 8 Pages 468-478
Chronic kidney disease (CKD) is a global public health problem, affecting over 10% of the world’s population and more than half of the population aged over 70 years, imposing major costs on healthcare systems. Although the primary causes of CKD include various diseases such as diabetes, glomerulonephritis, and acute kidney injury (AKI), the progression of CKD is mediated by a common pathological pathway, which is mainly characterized by fibrosis and chronic inflammation. In this process, resident fibroblasts in the kidney play crucial roles. Accumulating evidence highlights the existence of functional heterogeneity and plasticity of fibroblasts and their diverse roles in kidney disease progression and resolution. In addition to renal fibrosis, renal anemia and peritubular capillary loss, two major complications of progressive CKD, are also caused by dysfunction of resident fibroblasts. Furthermore, age-dependent alterations in fibroblast behavior also contribute to age-dependent unique pathological conditions. In this article, we describe the current understanding regarding the behaviors of fibroblasts in the kidney in health, disease, and aging.