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Therapeutic Advances in Mitochondrial Dysfunction and Oxidative Stress in Chronic Diseases

A special issue of Journal of Clinical Medicine (ISSN 2077-0383). This special issue belongs to the section "Clinical Laboratory Medicine".

Deadline for manuscript submissions: closed (30 October 2022) | Viewed by 5798

Special Issue Editors

Dr. Amrendra K. Ajay

E-Mail Website
Guest Editor
Renal Division, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA
Interests: kidney disease; DNA damage signaling; cell biology; cancer biology; transcription regulation; gene editing; cell therapy; drug development
Dr. Isaac K Sundar

E-Mail Website
Guest Editor
Division of Pulmonary Critical Care and Sleep Medicine, Department of Internal Medicine, University of Kansas Medical Center, Kansas City, KS, USA
Interests: circadian rhythms; lung inflammation; mitochondrial dysfunction; extracellular vesicles; novel biomarkers; respiratory toxicology
Dr. Krishna Prahlad Maremanda

E-Mail Website
Guest Editor
Renal Division, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA
Interests: mitochondria in health and disease; exosomes; theranostics; renal fibrosis and renal cell carcinoma; CRISPR therapeutics; inhalation toxicology; reproductive toxicology

Special Issue Information

Dear Colleagues,

Mitochondria are one of the most important organelles that mediate cellular homeostasis. Mitochondria are the major source of ROS (reactive oxygen species) production. Oxidative stress is often characterized by the excessive ROS production, which causes several cellular alterations including mitochondrial dysfunction. Accumulating evidence suggests that oxidative stress and mitochondrial dysfunctions play a major role in the pathogenesis of various chronic diseases in peripheral tissues such as the lung (e.g., COPD, fibrosis, asthma), kidney (e.g., chronic kidney disease), and other vital organs. The usage of antioxidants in treating various chronic diseases is well known and widely studied across the scientific community. Recent advances in targeted therapeutics (specifically mitochondrial therapeutics) have helped to understand the key role played by mitochondria in health and diseases. Mitochondrial-based theranostics (therapy and diagnostics) are of immense interest and are ever-growing in recent years. This Special Issue is aimed to understand and update the recent advancements in the area of “mitochondrial dysfunction and oxidative stress” in various chronic diseases. We look forward to receiving your contributions.

Dr. Amrendra K. Ajay
Dr. Isaac K Sundar
Dr. Krishna Prahlad Maremanda
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 100 words) can be sent to the Editorial Office for announcement on this website.

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. Journal of Clinical Medicine 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 2600 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
  • oxidative stress
  • chronic lung disease
  • kidney disease
  • therapeutics

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Published Papers (2 papers)

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Research

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15 pages, 2122 KiB  
Article
Peripheral Blood Mononuclear Cells Mitochondrial Respiration and Superoxide Anion after Heart Transplantation
by Abrar Alfatni, Anne-Laure Charles, François Sauer, Marianne Riou, Fabienne Goupilleau, Samy Talha, Alain Meyer, Emmanuel Andres, Michel Kindo, Jean-Philippe Mazzucotelli, Eric Epailly and Bernard Geny
J. Clin. Med. 2022, 11(23), 7247; https://doi.org/10.3390/jcm11237247 - 6 Dec 2022
Cited by 2 | Viewed by 1723
Abstract
Introduction: The mitochondrial function of circulating peripheral blood mononuclear cells (PBMCs) is an interesting new approach to cardiac diseases. Thus, PBMC’s mitochondrial respiration decreases in relation to heart failure severity. However, no data are available on heart-transplanted patients (Htx). Population and Methods: We [...] Read more.
Introduction: The mitochondrial function of circulating peripheral blood mononuclear cells (PBMCs) is an interesting new approach to cardiac diseases. Thus, PBMC’s mitochondrial respiration decreases in relation to heart failure severity. However, no data are available on heart-transplanted patients (Htx). Population and Methods: We determined PBMCs mitochondrial respiration by high-resolution respirometry (Oroboros Instruments) and superoxide anion production using electron paramagnetic resonance (Bruker-Biospin) in 20 healthy subjects and 20 matched Htx and investigated clinical, biological, echocardiographic, coronarography and biopsy characteristics. Results: PBMCs mitochondrial respiratory chain complex II respiration was decreased in Htx (4.69 ± 0.84 vs. 7.69 ± 1.00 pmol/s/million cell in controls and Htx patients, respectively; p = 0.007) and complex IV respiration was increased (24.58 ± 2.57 vs. 15.68 ± 1.67 pmol/s/million cell; p = 0.0035). Superoxide anion production was also increased in Htx (1.47 ± 0.10 vs. 1.15 ± 0.10 µmol/min; p = 0.041). The leucocyte-to-lymphocyte ratio was increased in Htx, whom complex II correlated with leucocyte number (r = 0.51, p = 0.02) and with the left ventricular posterior wall peak early diastolic myocardial velocity (r = −0.62, p = 0.005). Complex IV was increased in the two patients with acute rejection and correlated negatively with Htx’s isovolumetric relation time (r = −0.45, p = 0.045). Discussion: Although presenting with normal systolic function, Htx demonstrated abnormal PBMC’s mitochondrial respiration. Unlike immunosuppressive therapies, subclinical diastolic dysfunction might be involved in these changes. Additionally, lymphopenia might reduce complex II, and acute rejection enhances complex IV respirations. Conclusion: PBMC’s mitochondrial respiration appears modified in Htx, potentially linked to cellular shift, mild diastolic dysfunction and/or acute rejection. Full article
(This article belongs to the Special Issue Therapeutic Advances in Mitochondrial Dysfunction and Oxidative Stress in Chronic Diseases)
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Review

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21 pages, 2329 KiB  
Review
Mitochondrial Dysfunction: A Cellular and Molecular Hub in Pathology of Metabolic Diseases and Infection
by Tapan Behl, Rashita Makkar, Md. Khalid Anwer, Rym Hassani, Gulrana Khuwaja, Asaad Khalid, Syam Mohan, Hassan A. Alhazmi, Monika Sachdeva and Mahesh Rachamalla
J. Clin. Med. 2023, 12(8), 2882; https://doi.org/10.3390/jcm12082882 - 14 Apr 2023
Cited by 12 | Viewed by 3477
Abstract
Mitochondria are semiautonomous doubly membraned intracellular components of cells. The organelle comprises of an external membrane, followed by coiled structures within the membrane called cristae, which are further surrounded by the matrix spaces followed by the space between the external and internal membrane [...] Read more.
Mitochondria are semiautonomous doubly membraned intracellular components of cells. The organelle comprises of an external membrane, followed by coiled structures within the membrane called cristae, which are further surrounded by the matrix spaces followed by the space between the external and internal membrane of the organelle. A typical eukaryotic cell contains thousands of mitochondria within it, which make up 25% of the cytoplasm present in the cell. The organelle acts as a common point for the metabolism of glucose, lipids, and glutamine. Mitochondria chiefly regulate oxidative phosphorylation-mediated aerobic respiration and the TCA cycle and generate energy in the form of ATP to fulfil the cellular energy needs. The organelle possesses a unique supercoiled doubly stranded mitochondrial DNA (mtDNA) which encodes several proteins, including rRNA and tRNA crucial for the transport of electrons, oxidative phosphorylation, and initiating genetic repair processors. Defects in the components of mitochondria act as the principal factor for several chronic cellular diseases. The dysfunction of mitochondria can cause a malfunction in the TCA cycle and cause the leakage of the electron respiratory chain, leading to an increase in reactive oxygen species and the signaling of aberrant oncogenic and tumor suppressor proteins, which further alter the pathways involved in metabolism, disrupt redox balance, and induce endurance towards apoptosis and several treatments which play a major role in developing several chronic metabolic conditions. The current review presents the knowledge on the aspects of mitochondrial dysfunction and its role in cancer, diabetes mellitus, infections, and obesity. Full article
(This article belongs to the Special Issue Therapeutic Advances in Mitochondrial Dysfunction and Oxidative Stress in Chronic Diseases)
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