**1. Introduction**

Kidney diseases are a severe health problem that causes high economic costs worldwide in medical attention, emergency, therapies, among others [1,2]. These are divided into acute kidney injury (AKI) and chronic kidney diseases (CKD). AKI encompasses a set of pathologies characterized by the rapid loss of renal function in a short period [3]. AKI is often caused by the use of chemotherapeutics agents such as cisplatin, episodes of renal ischemia/reperfusion (I/R), and exposure to contaminants [4]. AKI is associated with high morbidity and mortality, contributing to CKD development and affecting approximately between 7% and 12% of the world [5]. CKD cause renal fibrosis development [6–8]. The latter comprises an unsatisfactory repair process and is the consequence of severe and persistent damage that does not restore organ function [9]. Renal fibrosis, in turn, is one of the principal mechanisms involved in AKI to CKD transition [5].

Mitochondria are responsible for several cell functions such as cell growth, cell survival, and apoptosis induction, playing a significant role in kidney physiology and the development of kidney diseases. Mitochondria also coordinate the biosynthesis of lipids, amino acids, and nucleotides and bioenergetics processes such as tricarboxylic acid (TCA) cycles, electron transport systems (ETSs), and fatty acids (FA) β-oxidation [10]. During

**Citation:** Aranda-Rivera, A.K.; Cruz-Gregorio, A.; Aparicio-Trejo, O.E.; Pedraza-Chaverri, J. Mitochondrial Redox Signaling and Oxidative Stress in Kidney Diseases. *Biomolecules* **2021**, *11*, 1144. https:// doi.org/10.3390/biom11081144

Academic Editor: Liang-Jun Yan

Received: 13 July 2021 Accepted: 1 August 2021 Published: 3 August 2021

**Publisher's Note:** MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations.

**Copyright:** © 2021 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https:// creativecommons.org/licenses/by/ 4.0/).

these processes, reactive oxygen species (ROS) are produced. Low levels of ROS are needed to regulate cellular signaling, but an excess of ROS induces oxidative stress (OS). OS causes oxidative damage in organelles including mitochondria and biomolecules, such as proteins, lipids, and deoxyribonucleic acid (DNA), which may be conducive to cell death. Indeed, OS is associated with AKI development and its transition to CKD, where mitochondria dysfunction is the principal characteristic of both [11,12]. Although mitochondrial metabolism, ROS production, and OS have been studied in kidney diseases, the role of redox signaling pathways in renal mitochondria impairment is not well understood. This review focuses on altering the metabolism and dynamics of mitochondria through the dysregulation of redox-sensitive signaling pathways in kidney diseases.
