Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
10.0
4.9
Journals
IJMS
Special Issues
Mitochondrial Dysfunction in Disease: Mechanisms, Biomarkers and Emerging Therapies
ijms-logo
Submit to Special Issue Submit Abstract to Special Issue Review for IJMS Propose a Special Issue

Journal Menu

► Journal Menu

Journal Browser

► Journal Browser
share announcement

Mitochondrial Dysfunction in Disease: Mechanisms, Biomarkers and Emerging Therapies

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

Deadline for manuscript submissions: 20 September 2026 | Viewed by 1126

Special Issue Editor

Dr. Alexandre Umpierrez Amaral

E-Mail Website
Guest Editor
Department of Biochemistry, Postgraduate Program in Biological Sciences, Biochemistry, Institute of Basic Health Sciences, Universidade Federal Do Rio Grande Do Sul, Porto Alegre, RS, Brazil
Interests: mitochondrial function; redox homeostasis; calcium homeostasis; oxidative stress; planarian; metabolic diseases
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Mitochondria are responsible for critical functions in the maintenance of cellular homeostasis. These organelles supply most of the ATP required for cell physiology, collaborate with the endoplasmic reticulum in maintaining low and controlled cytosolic calcium levels, and regulate redox homeostasis by generating and scavenging reactive oxygen species. Mitochondria are also involved in apoptosis, immune regulation, and metabolic reprogramming. A sophisticated regulatory network involving mitochondrial biogenesis, mitophagy, and dynamics plays a significant role in preserving the stability of mitochondrial structure and function. Therefore, damage to enzyme activities, protein functions, or mitochondrial quality control processes can produce dysfunctional mitochondria, possibly resulting in catastrophic events that disrupt bioenergetics, calcium, or redox homeostasis, ultimately leading to cell death.

A substantial body of evidence in recent decades has demonstrated that dysfunctional mitochondria contribute to numerous pathological processes involving a variety of tissues. Moreover, recent studies have targeted improvements in mitochondrial function as a potential therapeutic approach, opening new avenues for the treatment of mitochondrion-related diseases in the future.

We invite the submission of high-quality research and review articles to this Special Issue, which will synthesize current knowledge concerning the role of mitochondria in disease and novel therapies to restore mitochondrial function. Submissions may include both in vitro and in vivo studies using various experimental approaches, such as cellular and animal disease models. Clinical research is also welcome. 

We look forward to receiving your contributions.

Dr. Alexandre Umpierrez Amaral
Guest Editor

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. 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

  • mitochondria
  • bioenergetic homeostasis
  • calcium homeostasis
  • redox homeostasis
  • oxidative stress
  • biogenesis
  • mitophagy
  • dynamics

Benefits of Publishing in a Special Issue

  • Ease of navigation: Grouping papers by topic helps scholars navigate broad scope journals more efficiently.
  • Greater discoverability: Special Issues support the reach and impact of scientific research. Articles in Special Issues are more discoverable and cited more frequently.
  • Expansion of research network: Special Issues facilitate connections among authors, fostering scientific collaborations.
  • External promotion: Articles in Special Issues are often promoted through the journal's social media, increasing their visibility.
  • Reprint: MDPI Books provides the opportunity to republish successful Special Issues in book format, both online and in print.

Further information on MDPI's Special Issue policies can be found here.

Published Papers (2 papers)

Download All Papers
Order results
Result details
Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:

Research

Jump to: Other

15 pages, 2317 KB  
Article
Effects of Glyphosate and Roundup® Herbicides on Cardiac and H9c2 Cells’ Mitochondrial Respiration and Oxidative Stress
by Rayhana Rihani, Anne-Laure Charles, Walid Oulehri, Anne Lejay, Anne Charloux, Margherita Giannini, Alain Meyer and Bernard Geny
Int. J. Mol. Sci. 2026, 27(10), 4583; https://doi.org/10.3390/ijms27104583 - 20 May 2026
Viewed by 252
Abstract
Herbicides, used worldwide to improve agricultural yields, are associated with pollution and significant health problems. Cardiac damage is a major concern, and the respective contributions of glyphosate (GP) and its commercial formulation, Roundup® (RU), warrant investigation. We studied the specific effects of [...] Read more.
Herbicides, used worldwide to improve agricultural yields, are associated with pollution and significant health problems. Cardiac damage is a major concern, and the respective contributions of glyphosate (GP) and its commercial formulation, Roundup® (RU), warrant investigation. We studied the specific effects of GP and RU on isolated rat cardiac mitochondria and on H9c2 cardiomyocytes cultured for 6 and 24 h to determine whether the potential cardiotoxicity of GP and/or RU are linked to impaired mitochondrial respiration and increased hydrogen peroxide (H2O2) production. To this end, we used various mitochondrial complex substrates and a high-resolution oxygraphy. Unlike the GP alone which demonstrated no significant effect, the RU decreased cardiac mitochondrial respiration (21.90 ± 2.99 vs. 41.23 ± 7.09 pmol/s/mL, −46.9%, p = 0.007) for OXPHOS CI in respectively the RU and the control groups. RU also impaired OXPHOS CI+II (−51.5%, p = 0.003), maximal mitochondrial respiration (ETS CI+II, −46.7%, p = 0.001) and coupling (−35.4%, p = 0.0003). Similarly, 24 h exposure to RU decreased H9c2 cell number (−48.59%, p = 0.0023) but increased their mitochondrial respiration (+38.2%, p = 0.03, +37.6%, p = 0.03, +43.2%, p = 0.03 for OXPHOS CI, OXPHOS CI+II and ETS CI+II respectively). We observed a similar trend (NS) after 24 h exposure to GP. In conclusion, these results support an enhanced cardiac toxicity of the Roundup® as compared to the glyphosate. Both decreased mitochondrial respiration and increased hydrogen peroxide production were involved in isolated mitochondria impairment. After 24 h exposure to Roundup®, a compensatory mechanism potentially counterbalanced the decreased H9c2 cell number. These data support future studies aiming to reduce Roundup®-associated cardiac alterations not only by reducing its use but also by investigating the effectiveness of antioxidant and mitochondria-focused therapy. Full article
(This article belongs to the Special Issue Mitochondrial Dysfunction in Disease: Mechanisms, Biomarkers and Emerging Therapies)
►▼ Show Figures

Figure 1

Other

Jump to: Research

11 pages, 1283 KB  
Case Report
Diagnosing Metformin Intoxication with High-Resolution Platelet Respirometry: A Case Report
by Ondřej Sobotka, Pavla Staňková, Joao Fortunato, Eva Trčková and Pavel Skořepa
Int. J. Mol. Sci. 2026, 27(10), 4631; https://doi.org/10.3390/ijms27104631 - 21 May 2026
Viewed by 327
Abstract
Metformin-associated lactic acidosis (MALA) involves mitochondrial Complex I inhibition, traditionally diagnosed via indirect markers. We present platelet high-resolution respirometry (HRR) as a novel “liquid biopsy” to directly quantify metformin-induced systemic bioenergetic lesions. A 65-year-old diabetic male presented with severe lactic acidosis, acute kidney [...] Read more.
Metformin-associated lactic acidosis (MALA) involves mitochondrial Complex I inhibition, traditionally diagnosed via indirect markers. We present platelet high-resolution respirometry (HRR) as a novel “liquid biopsy” to directly quantify metformin-induced systemic bioenergetic lesions. A 65-year-old diabetic male presented with severe lactic acidosis, acute kidney injury, and profound hypoglycemia after intentionally overdosing on metformin (120 g), dapagliflozin (600 mg), and insulin glargine (300 U). While hemodialysis cleared plasma metformin and resolved the acidosis, refractory hypoglycemia required high-dose IV glucose for over six days. Day 2 platelet HRR revealed severe Complex I inhibition despite significantly decreased plasma metformin, indicating a profound “toxicodynamic lag.” Mitochondrial bioenergetics recovered by Day 7, reflecting natural platelet turnover. The protracted hypoglycemia was driven by a synergistic triad: metformin-inhibited gluconeogenesis, insulin glargine’s prolonged depot effect, and dapagliflozin-induced persistent renal glucose wasting. Platelet HRR has the potential to be a clinically applicable tool to reveal the “hidden” cellular phase of metformin toxicity missed by standard biomarkers. Furthermore, clinicians must anticipate severe, protracted hypoglycemia in mixed overdoses involving SGLT2 inhibitors. Full article
(This article belongs to the Special Issue Mitochondrial Dysfunction in Disease: Mechanisms, Biomarkers and Emerging Therapies)
►▼ Show Figures

Figure 1

Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:
 
Displaying articles 1-2
Back to TopTop