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The Role of Mitochondria in Renal and Cardiac Diseases

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: 31 May 2026 | Viewed by 240

Special Issue Editors


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Guest Editor
Department of Biology, Faculty of Chemistry, National Autonomous University of Mexico, Mexico City, Mexico
Interests: chronic kidney disease; cardiac diseases; antioxidants; mitochondria dysfunction

Special Issue Information

Dear Colleagues,

Renal and cardiac diseases represent a significant global burden, affecting one million people. These diseases converge in cardiorenal syndrome (CRS), known for inducing acute or chronic heart or kidney damage and affecting the other organ. The heart and kidneys depend on the mitochondria to produce 90% of ATP via fatty acid (FA) oxidation and oxidative phosphorylation (OXPHOS). Thus, alterations to this organelle lead to mitochondrial impairment, characterized by reduced bioenergetics, impaired biogenesis, and imbalanced dynamics. These processes cause oxidative stress, inflammation, and fibrosis, leading to organ dysfunction.

We are pleased to invite you to submit to this Special Issue focusing on the involvement of mitochondria in renal and cardiac diseases. We encourage work on the roles of mitochondrial ROS (mtROS), bioenergetics, dynamics, biogenesis, and mitochondrial metabolism.

This Special Issue will showcase the latest findings on mitochondrial dysfunction in renal or cardiac pathologies. We welcome original research articles and reviews focusing on (but not limited to) mitochondrial function, mitochondrial proteins, and mitochondrial alterations, including redox imbalance, mutations, dynamics, and bioenergetics impairment in renal and cardiac pathologies.

We look forward to receiving your contributions.

Dr. Ana Karina Aranda-Rivera
Prof. Dr. José Pedraza Chaverri
Guest Editors

Manuscript Submission Information

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Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • kidney and cardiac diseases
  • mitochondria
  • mitochondrial impairment
  • cardiorenal syndrome
  • mitochondrial proteins
  • dynamics
  • bioenergetics

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Published Papers (1 paper)

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Research

17 pages, 12764 KB  
Article
Omega-3 Fatty Acids Attenuate Renal Myostatin Expression and Mitochondrial Alterations Under Uremic Conditions
by Su Mi Lee, Yu In Jeong, Sumin Jung, Dong Eun Yang, Seo Hee Rha, Seong Eun Kim and Won Suk An
Int. J. Mol. Sci. 2026, 27(9), 4030; https://doi.org/10.3390/ijms27094030 - 30 Apr 2026
Abstract
Myostatin is associated with inflammatory processes; however, its renal expression and impact on mitochondrial homeostasis during chronic kidney disease (CKD) remain poorly defined. This study investigated whether omega-3 fatty acids (FAs) modulate renal myostatin and mitochondrial integrity under uremic conditions using both in [...] Read more.
Myostatin is associated with inflammatory processes; however, its renal expression and impact on mitochondrial homeostasis during chronic kidney disease (CKD) remain poorly defined. This study investigated whether omega-3 fatty acids (FAs) modulate renal myostatin and mitochondrial integrity under uremic conditions using both in vivo and in vitro models. In rats with adenine-induced CKD, omega-3 FA supplementation attenuated the increase in renal myostatin expression. Uremia was associated with impaired mitochondrial homeostasis, evidenced by decreased peroxisome proliferator-activated receptor gamma coactivator-1 alpha levels and increased dynamin-related protein 1 levels, alongside the upregulation of mitophagy and inflammatory markers. Furthermore, mitochondrial structural damage and reduced mitochondrial DNA (mtDNA) content were observed in uremic kidneys. Omega-3 FA treatment partially reversed these alterations, restored mtDNA levels, and preserved mitochondrial cristae integrity. In vitro, HK-2 cells treated with indoxyl sulfate exhibited increases in myostatin expression and mitochondrial impairment, which were mitigated by eicosapentaenoic acid, docosahexaenoic acid, or their combination. These findings suggest that omega-3 FAs exert protective effects against uremia-induced renal injury by suppressing myostatin and preserving mitochondrial homeostasis, specifically by modulating biogenesis, dynamics, and structural integrity. Consequently, omega-3 FAs may serve as a potential therapeutic strategy with which to preserve mitochondrial homeostasis in patients with CKD. Full article
(This article belongs to the Special Issue The Role of Mitochondria in Renal and Cardiac Diseases)
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