**8. Concluding Remarks**

ROS are second messengers that modify redox-sensitive proteins in mitochondria by inducing Ox-PTMs. Thus, low levels of ROS are necessary to render these modifications. However, in kidney diseases, ROS trigger mitochondrial dysfunction evident by alterations in FA β-oxidation, TCA cycle, OXPHOS, mitophagy, mitochondrial dynamics, and biogenesis.

Moreover, the crosstalk between NOXs and mitochondria generates ROS. The impairment in one of these elements can trigger an uncontrolled ROS production increase. Therefore, perturbations in mitochondrial redox homeostasis are common characteristics that allow the transition from AKI to CKD.

**Author Contributions:** Conceptualization, A.K.A.-R.; writing—original draft preparation, A.K.A.- R.; writing—review and editing, A.K.A.-R., A.C.-G., O.E.A.-T., and J.P.-C.; figures preparation, A.K.A.-R.; funding acquisition, J.P.-C. All authors have read and agreed to the published version of the manuscript.

**Funding:** This research was funded by Consejo Nacional de Ciencia y Tecnología (CONACYT; grant number: A1-S-7495) and by Dirección General de Asuntos del Personal Académico (DGAPA; grant numbers: IN202219 and IN200922).

**Institutional Review Board Statement:** Not applicable.

**Informed Consent Statement:** Not applicable.

**Data Availability Statement:** Not applicable.

**Acknowledgments:** A.K.A.-R. is a Ph.D. student from Posgrado en Ciencias Biológicas at the Universidad Nacional Autónoma de México and is recipient of a scholarship from CONACyT, México (CVU 818062). We gratefully acknowledge the Postdoctoral Grant's Program (POSTDOC) from the Dirección General de Asuntos Académicos (DGAPA), UNAM, for the postdoctoral fellow position to A.C.-G.

**Conflicts of Interest:** The authors declare no conflict of interest.

#### **Abbreviations**




