Abstract
In healthy kidneys, interstitial fibroblasts are responsible for the maintenance of renal architecture. Progressive interstitial fibrosis is thought to be a common pathway for chronic kidney diseases (CKD). Diabetes is one of the boosters of CKD. There is no effective treatment to improve kidney function in CKD patients. The kidney is a highly demanding organ, rich in redox reactions occurring in mitochondria, making it particularly vulnerable to oxidative stress (OS). A dysregulation in OS leads to an impairment of the Electron transport chain (ETC). Gene deficiencies in the ETC are closely related to the development of kidney disease, providing evidence that mitochondria integrity is a key player in the early detection of CKD. The development of novel CKD therapies is needed since current methods of treatment are ineffective. Antioxidant targeted therapies and metabolic approaches revealed promising results to delay the progression of some markers associated with kidney disease. Herein, we discuss the role and possible origin of fibroblasts and the possible potentiators of CKD. We will focus on the important features of mitochondria in renal cell function and discuss their role in kidney disease progression. We also discuss the potential of antioxidants and pharmacologic agents to delay kidney disease progression.
Highlights
The continuous decline of renal function is closely associated with progressive aberrant accumulation of Extracellular matrix (ECM) proteins such as fibronectin and collagen that culminates in fibrosis
There is no doubt that it is necessary to pay better attention to the condition of diabetes, even more when this pathology is associated with kidney problems, as these patients end up having a clinical worsening much sooner
The correction and or the prevention of mitochondrial dysfunction may be pivotal in the prevention and treatment of kidney disease
Summary
Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations. The continuous decline of renal function is closely associated with progressive aberrant accumulation of Extracellular matrix (ECM) proteins such as fibronectin and collagen that culminates in fibrosis. This progressive interstitial fibrosis is thought to be a common pathway for CKD [2]. Transition (EMT) in interstitial fibrosis, a process that is associated with multiple kidney diseases that result in irreversible loss of renal function. The paradigm of EMT plasticity will be elucidated, as well as signaling mediators and potential therapeutic targets to avoid progressive kidney disease at earlier stages, even those that await deeper biochemical understanding. We will unveil the possible role of mitochondria dysfunction in the pathogenesis of kidney disease and summarize the recent development of mitochondria-targeted therapies
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