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New Insights into Mitochondria in Health and Disease
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New Insights into Mitochondria in Health and Disease

A Special Issue of Biology (ISSN 2079-7737) belonging to the section "Medical Biology".

Deadline for manuscript submissions: 31 December 2026 | Viewed by 3594

Editor

Dr. Huiliang Zhang

E-Mail Website
Guest Editor
Department of Medical Genetics and Molecular Biochemistry, Temple University, Philadephia, PA 19140, USA
Interests: mitochondria; aging; heart dysfunction; neuron degenerative disease; drug development
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Biology is calling for submissions to our Special Issue on mitochondria in health and diseases. Mitochondria not only work in energy production but also play important roles in reactive oxygen species (ROS) production, calcium handling, metabolism, cell signaling, etc. They have been increasingly recognized as important players in the aging and disease processes. Mitochondrial dysfunction is one of the hallmarks of aging and diseases, including cardiovascular dysfunction, neuron degenerative diseases, skeletal muscle decline, kidney dysfunction, skin aging, immune dysfunction, stem cell dysfunction, etc. There is an urgent need to elucidate the mechanisms of mitochondrial dysfunction and seek mitochondrial-targeted treatments in aging and disease. In this Special Issue, we welcome submissions of original research, reviews, and mini-reviews. Subtopics of interests include, but are not limited to, the following:

  1. Mitochondrial bioenergetics and metabolism.
  2. Mitochondrial dynamics, DNA damage, Ca2+ handling, reactive species (ROS and RNS) production, and metabolism disorder.
  3. Mitochondrial dysfunction in cell dysfunction and diseases, such as stem cell dysfunction, skeletal muscle disease, cardiovascular disease, neurodegenerative disease, Alzheimer’s diseases and related dementia, etc.
  4. Mitochondria in inflammation and immune dysfunction. 
  5. Mitochondrial quality control.
  6. Epigenetic regulation and potential targets in mitochondria
  7. Other mitochondria-related dysfunction in aging and disease research.

Dr. Huiliang Zhang
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-anonymized peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Biology is an international peer-reviewed open access semimonthly 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

  • mitochondria
  • cell dysfunction
  • aging
  • diseases

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

Published Papers (2 papers)

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Research

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19 pages, 17335 KB  
Article
Mitochondrial-Targeted SS-31 Attenuates the Doxorubicin-Induced Cardiomyoblast H9C2 Cell Senescence
by Jiaojiao Fan, Jinzi Wu, Shuo Yan, Songlin Li, Peter S. Rabinovitch, Xingyun Qi and Huiliang Zhang
Biology 2026, 15(13), 1034; https://doi.org/10.3390/biology15131034 - 28 Jun 2026
Viewed by 757
Abstract
Doxorubicin (DOX), an effective chemotherapeutic agent for many types of cancer, is known for significant cardiotoxic side effects, which largely limit its clinical usage. A 3 h treatment of cardiomyoblast H9C2 cells with a low concentration of DOX (100 nM) can induce senescence-associated [...] Read more.
Doxorubicin (DOX), an effective chemotherapeutic agent for many types of cancer, is known for significant cardiotoxic side effects, which largely limit its clinical usage. A 3 h treatment of cardiomyoblast H9C2 cells with a low concentration of DOX (100 nM) can induce senescence-associated β-galactosidase (SA β-gal) staining, a gold standard of cell senescence. In the current study, we comprehensively characterized the phenotype of the DOX-induced senescent cardiomyocytes for the first time. Establishing this in vitro model will facilitate an expanded capacity for searching for effective treatments for DOX-induced cell senescence. Using SA β-gal staining and cell growth rate as readouts, we assessed the concentration-dependent effect of DOX on H9C2 cell senescence. The cells were treated with DOX for 3 h and subsequently cultured for 3 days. We found that a 50 nM concentration of DOX induced ~50% SA β-gal staining and completely inhibited cell growth. The DOX-induced H9C2 cell senescence was further confirmed by several well-accepted senescence markers, including cell hypertrophy, increased p16 and p21 expression, increased Senescence Associated Secretory Phenotype (SASP) markers, arrested cell cycle, and increased ROS production. Interestingly, we found that 50 nM DOX increased mitochondrial respiration. Translationally, we found that mitochondrial-targeted tetrapeptide SS-31 (elamipretide, 1 µM) partially attenuated 50 nM DOX-induced SA β-gal staining from 51.4% to 35.8%. SS-31 also prevented increases in the p16, p21, and SASP markers and mitigated mitochondrial ROS production. Additionally, SS-31 reversed the 50 nM DOX-induced elevation of mitochondrial respiration. However, 1 µM SS-31 failed to prevent the cell cycle arrest induced by 50 nM DOX. Using a 3 h treatment of 50 nM DOX, we established an H9C2 cell senescence model. Treatment with SS-31 attenuates this DOX-induced cell senescence but not the cell cycle arrest. These data suggest that SS-31 is a promising drug to treat DOX-induced cardiomyocyte senescence. Full article
(This article belongs to the Special Issue New Insights into Mitochondria in Health and Disease)
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Review

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33 pages, 3117 KB  
Review
The Therapeutic Crossroad Between Mitochondria and Cannabidiol: A Mini-Review
by Mihaela Jorgovan, Tamara Maksimović, Oana Bătrîna, Codruța Șoica, Alexandra Mioc and Marius Mioc
Biology 2026, 15(6), 510; https://doi.org/10.3390/biology15060510 - 22 Mar 2026
Cited by 1 | Viewed by 2351
Abstract
Cannabidiol is a non-psychoactive compound originating from Cannabis sativa L., with a promising therapeutic profile that influences numerous cellular processes. A major area of interest is its impact on mitochondria, organelles essential for cellular metabolism, ATP production, calcium homeostasis, and stress response. This [...] Read more.
Cannabidiol is a non-psychoactive compound originating from Cannabis sativa L., with a promising therapeutic profile that influences numerous cellular processes. A major area of interest is its impact on mitochondria, organelles essential for cellular metabolism, ATP production, calcium homeostasis, and stress response. This article explores the available data on contribution of CBD effect on mitochondria to its therapeutic potential in treatment of various pathologies: cancer, cardiovascular, lung, neurological, gastrointestinal and liver disease, and muscle pathologies. Regarding cancer, the cytotoxic effects of cannabidiol on glioma, leukaemia, non-Hodgkin lymphoma, prostate, gastric, and breast cancer are analysed. In the case of cardiomyopathies and heart failure, cannabidiol plays an important role in reducing oxidative stress and promoting mitochondrial biogenesis. In lung diseases, cannabidiol reduces the expression of mitochondrial fission genes and increases the expression of fusion genes. When it comes to neurological pathologies, cannabidiol protects neurons and exhibits a strong antioxidant effect, while in gastrointestinal and liver diseases, cannabidiol stabilises mitochondrial membrane potential, increases ATP production, and reduces oxidative stress. In muscle affections, cannabidiol improves mitochondrial function by inhibiting excessive mitophagy. Although modern formulations may improve the low bioavailability of CBD, its potential non-selective cytotoxicity toward non-malignant cells remains an important concern that warrants further investigation. Nevertheless, cannabidiol possesses a remarkable therapeutic potential, and its effects on mitochondria open new perspectives in the treatment of numerous diseases. Full article
(This article belongs to the Special Issue New Insights into Mitochondria in Health and Disease)
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