Journal of Clinical Nephrology and Therapeutics

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Short Communication - Journal of Clinical Nephrology and Therapeutics (2025) Volume 9, Issue 1

The impact of mitochondrial dysfunction on renal injury: Mechanisms and therapeutic insights

Jay Wish >*

Department of Renal Medicine, University College London, UK

*Corresponding Author:
Jay Wish
Department of Renal Medicine, University College London, UK
Institute of Nephrology Research
USA
E-mail: jay@wish.edu

Received:02-Feb-2024,Manuscript No. AACNT-24-161910; Editor assigned:03-Feb-2024,PreQC No. AACNT-24-161910(PQ); Reviewed:16-Feb-2024,QC No. AACNT-24-161910; Revised:20-Feb-2024,Manuscript No. AACNT-24-161910(R); Published:27-Feb-2024,DOI: 10.35841/aacnt-9.1.247

Citation: : Wish J. The impact of mitochondrial dysfunction on renal injury: Mechanisms and therapeutic insights. J Clini Nephrol. 2025; 9(1):247

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Introduction

Mitochondria play a fundamental role in cellular energy metabolism, oxidative stress regulation, and apoptosis. The kidneys, due to their high energy demands, are particularly reliant on mitochondrial function for optimal performance. Any disruption in mitochondrial dynamics can contribute to renal injury, leading to acute kidney injury (AKI) and chronic kidney disease (CKD). This article explores the relationship between mitochondrial dysfunction and renal pathology, detailing the mechanisms involved and potential therapeutic approaches [1].

Mitochondria are the powerhouse of renal cells, particularly in the proximal tubules, where high levels of ATP are required for active transport processes. Mitochondrial homeostasis ensures proper cellular respiration, ion balance, and toxin filtration. However, when mitochondrial integrity is compromised, renal function deteriorates, setting the stage for progressive kidney damage [2].

Mitochondrial dysfunction in renal injury arises from several interconnected mechanisms, including oxidative stress, impaired mitochondrial biogenesis, and disrupted mitophagy. Excessive reactive oxygen species (ROS) production due to dysfunctional mitochondria leads to lipid peroxidation, protein oxidation, and DNA damage, which collectively exacerbate renal cell injury and inflammation [3].

Oxidative stress generated by dysfunctional mitochondria triggers an inflammatory response in kidney tissues. Activation of inflammatory pathways, such as the NF-κB and NLRP3 inflammasome, amplifies renal damage by promoting fibrosis and cell apoptosis. Chronic inflammation contributes to the progression of kidney diseases, making oxidative stress management a crucial therapeutic target [4].

Mitochondrial biogenesis, regulated by peroxisome proliferator-activated receptor gamma coactivator-1 alpha (PGC-1α), is a vital process for maintaining mitochondrial health. In renal diseases, reduced PGC-1α expression leads to defective mitochondrial regeneration and worsened kidney function. Enhancing mitochondrial biogenesis through pharmacological and lifestyle interventions holds promise in mitigating renal injury [5].

Mitophagy, the selective degradation of damaged mitochondria, is essential for preventing the accumulation of dysfunctional organelles. Impaired mitophagy results in mitochondrial debris accumulation, further exacerbating renal injury. Therapeutic strategies targeting mitophagy regulation, such as autophagy-inducing agents, could serve as potential interventions for kidney disease [6].

Acute kidney injury (AKI) is often associated with mitochondrial damage due to ischemia-reperfusion injury, nephrotoxins, and sepsis. In contrast, chronic kidney disease (CKD) involves progressive mitochondrial impairment, contributing to renal fibrosis and organ failure. Understanding the mitochondrial pathophysiology in both conditions is crucial for developing effective treatments [7].

Several therapeutic strategies aim to restore mitochondrial function in renal disease. Antioxidants such as coenzyme Q10, N-acetylcysteine, and MitoQ have shown promise in reducing oxidative stress and improving mitochondrial efficiency. Additionally, mitochondrial transplantation and gene therapy are emerging as potential interventions to repair damaged mitochondria in renal disorders [8].

Beyond pharmacological treatments, lifestyle modifications, including caloric restriction, exercise, and ketogenic diets, have been suggested to improve mitochondrial function in kidney disease. These interventions enhance mitochondrial biogenesis, reduce oxidative stress, and support overall renal health [9, 10].

Conclusion

Mitochondrial dysfunction is a central contributor to renal injury, playing a crucial role in both acute and chronic kidney diseases. Understanding the underlying mechanisms of mitochondrial damage, including oxidative stress, impaired biogenesis, and defective mitophagy, can pave the way for targeted therapeutic approaches. Future research into mitochondrial-targeted treatments and lifestyle interventions holds great potential for improving kidney health and reducing the burden of renal diseases worldwide.

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