Mitochondrial Dysfunction in the Cardio-Renal Axis
Nerea Mendez-Barbero1,2, Jorge Oller1,2, Ana B Sanz3,4
1Laboratory of Vascular Pathology, IIS-Fundación Jiménez Díaz, 28040 Madrid, Spain.
Insights
Cardiovascular disease and chronic kidney disease together, known as cardio-renal syndrome, significantly increase mortality. Mitochondrial dysfunction is key, suggesting therapies targeting mitochondrial homeostasis could treat this condition.
Area of Science:
- Mitochondrial biology
- Cardiovascular medicine
- Nephrology
Background:
- Cardiovascular disease (CVD) often complicates chronic kidney disease (CKD), leading to cardio-renal syndrome (CRS).
- Patients with both conditions face a 20% to 500% increased risk of all-cause mortality.
- Mitochondrial dysfunction is implicated in both cardiovascular and renal pathologies.
Purpose of the Study:
- To review the role of mitochondrial homeostasis malfunction in CRS.
- To explore how mitochondrial dysfunction contributes to vascular pathologies in CKD and vice versa.
- To guide the development of novel therapeutic strategies for CRS.
Main Methods:
- Literature review of preclinical studies.
- Analysis of mitochondrial homeostasis pathways: biogenesis, dynamics, oxidative stress, and mitophagy.
- Examination of the interplay between kidney injury and vascular pathologies.
Main Results:
- Mitochondrial dysfunction is a central mechanism in CRS development and progression.
- Impaired mitochondrial biogenesis, dynamics, oxidative stress, and mitophagy contribute to vascular damage.
- Understanding these mechanisms offers insights into therapeutic interventions.
Conclusions:
- Maintaining mitochondrial homeostasis is a promising therapeutic strategy for CRS.
- Targeting mitochondrial pathways may mitigate the adverse effects of cardio-renal interactions.
- Further research into mitochondrial mechanisms can inform novel CRS treatments.
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.
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