Mitochondrial bioenergetics, redox state, dynamics and turnover alterations in renal mass reduction models of chronic kidney diseases and their possible implications in the progression of this illness

Abstract

Nowadays, chronic kidney disease (CKD) is considered a worldwide public health problem. CKD is a term used to describe a set of pathologies that structurally and functionally affect the kidney, it is mostly characterized by the progressive loss of kidney function. Current therapeutic approaches are insufficient to avoid the development of this disease, which highlights the necessity of developing new strategies to reverse or at least delay CKD progression. Kidney is highly dependent on mitochondrial homeostasis and function, consequently, the idea that mitochondrial pathologies could play a pivotal role in the genesis and development of kidney diseases has risen. Although many research groups have recently published studies of mitochondrial function in acute kidney disease models, the existing information about CKD is still limited, especially in renal mass reduction (RMR) models. This paper focuses on reviewing current experimental information about the bioenergetics, dynamics (fission and fusion processes), turnover (mitophagy and biogenesis) and redox mitochondrial alterations in RMR, to discuss and integrate the mitochondrial changes triggered by nephron loss, as well as its relationship with loss of kidney function in CKD, in these models. Understanding these mechanisms would allow us to design new therapies that target these mitochondrial alterations.

Keywords: Adenosine triphosphate (CID 5957); Chronic kidney disease; Curcumin (CID 969516); Elamipretide: Szeto–Schiller peptides 31 (CID 11764719); Glutathione (CID 124886); L-cysteine (CID 60960); L-glutamate (CID 33032); Malate (CID 525); Mitochondria bioenergetics; Mitochondrial dynamic; Nephrectomy; Oxidative stress; Renal mass reduction; Resveratrol (CID 445154); Rotenone (CID 6758); Succinate (CID 1110).