Abstract
Chronic kidney disease (CKD) is a worldwide health problem affecting 9.1% of the world’s population. The treatments to prevent the progression of CKD remain limited, however. Resident fibroblasts in the kidneys play crucial roles in the pathological conditions commonly recognized in CKD, such as renal fibrosis, renal anemia, and peritubular capillary loss. Fibroblasts in the kidney provide structural backbone by producing extracellular matrix proteins and produce erythropoietin for normal hematopoiesis under physiological conditions. In the diseased condition, however, fibroblasts differentiate into myofibroblasts that produce excessive extracellular matrix proteins at the cost of the inherent erythropoietin-producing abilities, resulting in renal fibrosis and renal anemia. Pericytes, which are mesenchymal cells that enwrap peritubular capillaries and highly overlap with resident fibroblasts, detach from peritubular capillary walls in response to kidney injury, resulting in peritubular capillary loss and tissue hypoxia. Several reports have demonstrated the beneficial roles of fibroblasts in the regeneration of renal tubules Renal fibroblasts also have the potential to differentiate into a proinflammatory state, producing various cytokines and chemokines and prolonging inflammation by forming tertiary lymphoid tissues, functional lymphoid aggregates, in some pathological conditions. In this article, we describe the heterogenous functions of renal fibroblasts under healthy and diseased conditions.
Highlights
Chronic kidney disease (CKD) is a worldwide public health problem
Previous studies have shown that dysfunction of the renal fibroblasts can induce several pathological conditions associated with CKD, such as renal fibrosis, renal anemia, and peritubular capillary loss
Myofibroblasts mainly contribute to renal fibrosis and deteriorate renal function by producing excessive extracellular matrix (ECM), they can have host-protective roles in the early phase of kidney injury
Summary
Chronic kidney disease (CKD) is a worldwide public health problem. In 2017, the prevalence of CKD was estimated to be 9.1% in the world’s population, and has increased by 29.3% from 1990 to 2017 [1]. Patients with ESRD need renal replacement therapies such as dialysis and renal transplantation to survive The cost of these therapies is enormous and the financial burden is a critical problem for patients and society [4]. In diseased kidneys, fibroblasts lose these physiological functions and transdifferentiate into myofibroblasts These phenotypic changes result in fibrosis, renal anemia, and peritubular capillary loss, all of which are common pathological conditions of CKD, irrespective of the etiology [6]. Fibroblasts play a crucial role in prolonging inflammation by inducing tertiary lymphoid tissue (TLT) formation [8]. These features highlight the importance of understanding the behavior of fibroblasts in the kidney in order to identify efficient therapeutic strategies to prevent CKD progression. We describe the current understanding of the heterogeneous functions of fibroblasts in healthy and diseased kidneys
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