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Biomolecules
Special Issues
Acute Kidney Injury and Mitochondrial Involvement
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Acute Kidney Injury and Mitochondrial Involvement

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Chemical Biology".

Deadline for manuscript submissions: 31 May 2026 | Viewed by 5459

Special Issue Editors

Dr. Iva Suman

E-Mail Website1 Website2
Guest Editor
Faculty of Medicine, University of Rijeka, Braće Branchetta 20, 51000 Rijeka, Croatia
Interests: kidney injury; apoptosis; mitophagy; autophagy; oxidative stress; cell signaling; mitochondria
Special Issues, Collections and Topics in MDPI journals
Dr. Alenka Višnić

E-Mail Website
Guest Editor
Department of Human Reproduction, Clinic for Gynecology and Obstetrics, Clinical Hospital Center Rijeka, 51000 Rijeka, Croatia
Interests: biomarkers of disease; mitochondria; endometriosis

Special Issue Information

Dear Colleagues,

There is still a high rate of morbidity and mortality associated with acute kidney injury (AKI), making it a significant challenge around the globe. Increasing evidence suggests that mitochondrial dysfunction plays an important role in the pathogenesis of AKI, affecting mitochondrial energetics, oxidative stress, and programmed cell death. Novel therapeutic strategies and diagnostic biomarkers may be developed by understanding the molecular mechanisms linking mitochondrial impairment to AKI.

This Special Issue on "Acute Kidney Injury and Mitochondrial Involvement" gathers the most recent research and reviews on mitochondrial biology in relation to AKI. It is our pleasure to welcome contributions exploring mitochondrial dynamics, metabolic reprogramming, mitophagy, and targeted interventions related to mitochondrial dynamics in preclinical settings. Researchers are invited to share their insights in the form of both research and review articles to advance our knowledge and improve outcomes for patients with AKI.

Dr. Iva Suman
Dr. Alenka Višnić
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 250 words) can be sent to the Editorial Office for assessment.

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. Biomolecules is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). 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

  • acute kidney injury

  • mitochondrial dysfunction

  • mitochondrial dynamics

  • mitophagy

  • biomarkers

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Published Papers (4 papers)

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Research

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21 pages, 3016 KB  
Article
Dose- and Organ-Specific Dual Effects of MitoTempo in Paracetamol-Induced Hepatorenal Toxicity in Mice
by Hilmi Orhan, Kemal Atmaca, Berin Aladağ and Mustafa Kotmakçı
Biomolecules 2026, 16(4), 556; https://doi.org/10.3390/biom16040556 - 9 Apr 2026
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Abstract
Paracetamol (PAR) overdose is a major cause of drug-induced liver injury and is also associated with renal toxicity, both involving mitochondrial dysfunction and oxidative stress. This study investigated the dose- and organ-specific effects of the mitochondria-targeted antioxidant MitoTempo (MT) on PAR-induced hepatorenal toxicity [...] Read more.
Paracetamol (PAR) overdose is a major cause of drug-induced liver injury and is also associated with renal toxicity, both involving mitochondrial dysfunction and oxidative stress. This study investigated the dose- and organ-specific effects of the mitochondria-targeted antioxidant MitoTempo (MT) on PAR-induced hepatorenal toxicity in mice. Male C57BL/6J mice received a single toxic dose of PAR (600 mg/kg), either alone or combined with MT (20 or 40 mg/kg). Twenty-four hours after treatment, serum markers of liver and kidney injury were measured, and mitochondrial function was assessed in both organs. PAR administration caused severe liver injury and moderate renal dysfunction, accompanied by increased mitochondrial oxidative stress, glutathione imbalance, mitochondrial permeability transition pore opening, and disruption of electron transport chain (ETC) integrity. MT co-treatment attenuated several PAR-induced mitochondrial alterations in a dose- and tissue-dependent manner; however, MT did not consistently confer protection and, in some settings, exacerbated oxidative stress and bioenergetic dysfunction, particularly in the kidney. Notably, recovery of ETC protein levels by MT was not consistently associated with restoration of enzymatic activity. Overall, these findings demonstrate that MT exerts dual, dose- and organ-specific effects on PAR-induced mitochondrial dysfunction, highlighting that mitochondria-targeted antioxidants are not universally protective. Full article
(This article belongs to the Special Issue Acute Kidney Injury and Mitochondrial Involvement)
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16 pages, 1683 KB  
Article
Mitigation of Ischemia/Reperfusion-Induced Acute Kidney Injury by Canagliflozin Is Associated with Altered Mitochondrial Dynamics and Reduced Proliferation in Swine
by Zaria K. Killingsworth, Malikeya Chaudhary, John A. Mares, Hengying Ellery, Cassie J. Rowe, Ian J. Stewart, Patrick F. Walker and David M. Burmeister
Biomolecules 2026, 16(2), 279; https://doi.org/10.3390/biom16020279 - 10 Feb 2026
Viewed by 699
Abstract
Increasing evidence implicates mitochondrial/cellular dynamics in ischemia reperfusion (I/R)-induced acute kidney injury (AKI). Sodium-glucose-co-transporter-2 inhibitors (SGLT2is, e.g., canagliflozin, CG) have been shown to mitigate I/R-induced AKI. Here, we hypothesized that CG-improved AKI was associated with altered mitochondrial dynamics and apoptosis in a previously [...] Read more.
Increasing evidence implicates mitochondrial/cellular dynamics in ischemia reperfusion (I/R)-induced acute kidney injury (AKI). Sodium-glucose-co-transporter-2 inhibitors (SGLT2is, e.g., canagliflozin, CG) have been shown to mitigate I/R-induced AKI. Here, we hypothesized that CG-improved AKI was associated with altered mitochondrial dynamics and apoptosis in a previously established swine model. CG (300 mg, PO) significantly increased pro-apoptotic genes Bid, Bad, Bax, Bak1 and Casp1 expression (all p < 0.05). Pink1 (p = 0.0019), Optn (p = 0.038), and Map1lc3 (p = 0.0093) expression also increased with CG, implicating mitophagy; PINK1 protein levels were unchanged. The expression of mitochondrial fission regulator Fis1 increased with CG treatment (p = 0.0015) while fusion regulator Opa1 expression decreased (p = 0.038). TUNEL staining showed increased apoptosis primarily in damaged proximal tubular cells of CG animals. Ki67 staining revealed I/R-injury increased cell proliferation throughout the kidney, which was significantly attenuated with CG. Moreover, correlative analysis revealed that AKI severity positively correlated with cell proliferation. In this large animal model, CG reduced AKI via increased mitochondrial fission and pro-apoptotic gene expression, potentiating clearance of damaged mitochondria, and decreased cell proliferation. Future studies should evaluate other SGLT2is as a potential therapeutic for I/R AKI. Full article
(This article belongs to the Special Issue Acute Kidney Injury and Mitochondrial Involvement)
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Review

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20 pages, 1399 KB  
Review
Mitochondrial Dysfunction in Acute Kidney Injury: Intersections Between Chemotherapy and Novel Cancer Immunotherapies
by Zaroon Zaroon, Carlotta D’Ambrosio and Filomena de Nigris
Biomolecules 2026, 16(1), 120; https://doi.org/10.3390/biom16010120 - 12 Jan 2026
Viewed by 1279
Abstract
Acute kidney injury (AKI) remains a major clinical challenge, with high morbidity and limited therapeutic options. In recent years, mitochondria have gained considerable attention as key regulators of the metabolic and immune responses during renal injury. Beyond their classical role in ATP production, [...] Read more.
Acute kidney injury (AKI) remains a major clinical challenge, with high morbidity and limited therapeutic options. In recent years, mitochondria have gained considerable attention as key regulators of the metabolic and immune responses during renal injury. Beyond their classical role in ATP production, mitochondria participate directly in inflammatory signaling, releasing mitochondrial DNA and other DAMPs that activate pathways such as TLR9, cGAS–STING, and the NLRP3 inflammasome. At the same time, immune cells recruited to the kidney undergo significant metabolic shifts that influence whether injury progresses or resolves. Increasing evidence also shows that immune-modulating therapies, including immune checkpoint inhibitors and innovative cell-based immunotherapies, can influence mitochondrial integrity, thereby altering renal susceptibility to injury. This review first summarizes the established knowledge on mitochondrial dysfunction in AKI, with emphasis on distinct mechanistic pathways activated by chemotherapy and immunotherapy. It then discusses emerging mitochondrial-targeted therapeutic strategies, logically integrating preclinical insights with data from ongoing and proposed clinical trials to present a coherent translational outlook. Full article
(This article belongs to the Special Issue Acute Kidney Injury and Mitochondrial Involvement)
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17 pages, 813 KB  
Review
Kidney Stone Disease: Epigenetic Dysregulation in Homocystinuria and Mitochondrial Sulfur Trans-Sulfuration Ablation Driven by COVID-19 Pathophysiology
by Anmol Babbarwal, Mahavir Singh, Utpal Sen, Mahima Tyagi and Suresh C. Tyagi
Biomolecules 2025, 15(8), 1163; https://doi.org/10.3390/biom15081163 - 14 Aug 2025
Viewed by 2338
Abstract
The coronavirus disease 2019 (COVID-19) pandemic, caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has brought to light unexpected complications beyond respiratory illness, including effects on kidney function and a potential link to kidney stone disease (KSD). This review proposes a novel [...] Read more.
The coronavirus disease 2019 (COVID-19) pandemic, caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has brought to light unexpected complications beyond respiratory illness, including effects on kidney function and a potential link to kidney stone disease (KSD). This review proposes a novel framework connecting COVID-19-induced epigenetic reprogramming to disruptions in mitochondrial sulfur metabolism and the pathogenesis of kidney stones. We examine how SARS-CoV-2 interferes with host methylation processes, leading to elevated homocysteine (Hcy) levels and impairment of the trans-sulfuration pathway mechanisms particularly relevant in metabolic disorders such as homocystinuria. These epigenetic and metabolic alterations may promote specific kidney stone subtypes through disrupted sulfur and oxalate handling. Additionally, we explore the role of COVID-19-associated gut dysbiosis in increasing oxalate production and driving calcium oxalate stone formation. Together, these pathways may accelerate the transition from acute kidney injury (AKI) to chronic KSD, linking viral methylation interference, sulfur amino acid imbalance, mitochondrial dysfunction, and microbiota changes. Unlike earlier reviews that address these mechanisms separately, this work offers an integrated hypothesis to explain post-viral renal lithogenesis and highlights the potential of targeting sulfur metabolism and redox pathways as therapeutic strategies for KSD triggered or aggravated by viral infections such as COVID-19. Full article
(This article belongs to the Special Issue Acute Kidney Injury and Mitochondrial Involvement)
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