Mitochondrial Dysfunction in the Cardio-Renal Axis

Int J Mol Sci. 2023 May 3;24(9):8209. doi: 10.3390/ijms24098209.

Abstract

Cardiovascular disease (CVD) frequently complicates chronic kidney disease (CKD). The risk of all-cause mortality increases from 20% to 500% in patients who suffer both conditions; this is referred to as the so-called cardio-renal syndrome (CRS). Preclinical studies have described the key role of mitochondrial dysfunction in cardiovascular and renal diseases, suggesting that maintaining mitochondrial homeostasis is a promising therapeutic strategy for CRS. In this review, we explore the malfunction of mitochondrial homeostasis (mitochondrial biogenesis, dynamics, oxidative stress, and mitophagy) and how it contributes to the development and progression of the main vascular pathologies that could be affected by kidney injury and vice versa, and how this knowledge may guide the development of novel therapeutic strategies in CRS.

Keywords: cardiovascular disease; kidney disease; mitochondrial dysfunction; oxidative stress; treatment.

Publication types

  • Review

MeSH terms

  • Cardio-Renal Syndrome*
  • Heart
  • Humans
  • Kidney / metabolism
  • Mitochondria
  • Renal Insufficiency, Chronic* / metabolism

Grants and funding

This research was funded by grants from the Instituto de Salud Carlos III (ISCIII) and Fondos FEDER European Union (PI20/00140, PI19/00815, and DTS20/00083, PI19/00588, PI19/00815, PI22/00469, PI22/00050, PI18/01133, PI21/01453, PI21/01126, Red de Investigación Renal REDINREN: RD16/0009/0003, and RICORS2040; RD21/0005/0002, RD21/0005/0001) funded by European Union—NextGenerationEU, Sociedad Española de Nefrología, Sociedad española de aterosclerosis (FEA 2021-BIB 05-21), and 2021 PREMIOS A LA INVESTIGACIÓN L’ORÉAL-UNESCO For Women in Science. Innovation programme under the Marie Skłodowska-Curie grant of the European Union’s Horizon 2020 (IMProve-PD ID: 812699) to M.R.-O., and the Juan de la Cierva incorporacion grant: IJC2018-035187-I to S.R.-M. J.O. is supported by a Ramón y Cajal contract (RYC2021-033343-I), from the Spanish Ministry of Science and Innovation and granted by Fundación MERCK—“Fundación FEDER de investigación clínica en enfermedades raras 2022” and by “V-Ayudas Muévete por los que no pueden 2021”. A.B.S was supported by the MICINN Ramon y Cajal program. The ISCIII Miguel Servet program supported N.M.-B.