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Biomedicines
Special Issues
Mitochondrial Function in Biomedicines
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Mitochondrial Function in Biomedicines

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Cell Biology and Pathology".

Deadline for manuscript submissions: closed (31 July 2023) | Viewed by 5018

Special Issue Editor

Dr. Paresh Prajapati

E-Mail Website
Guest Editor
Spinal Cord and Brain Injury Research Center, Department of Neuroscience, University of Kentucky, Lexington, KY 40536, USA
Interests: miRNAs; mitochondria

Special Issue Information

Dear Colleagues,

Advanced research in cell biology and medicine has revealed the multiple roles of mitochondria beyond energy production that are crucial for cell survival. Mitochondria are acknowledged as the core organelles associated with cellular homeostasis, and their dysfunction results in a wide range of mitochondria-associated disorders/diseases in humans.

Mitochondria are known to communicate with each other, undergo function-defining shape changes, regulate synaptic transmission, serve as a communication bridge between two distal parts of neurons, modulate transcriptional remodeling within the nucleus, systemically trigger inflammatory signaling following stress, release components associated with oncogenic transformation, and serve as core organelles to modulate complex biological systems. The mechanisms behind pathogenesis associated with bioenergetic and quality control aspects of mitochondria are now largely studied across large groups of biomedical disciplines, including oncology, immunology, genetics, neurotrauma, neurology, virology, regenerative medicine, and critical care medicine. An approach toward the understanding of the mitochondrial-mediated signaling pathways in human disorders/diseases has provided new prospects for diagnosis, prevention, therapy, and other fields of biomedicine.

This Special Issue of Biomedicines on "Mitochondrial Function in Biomedicines" will involve all aspects of better understanding mitochondrial targeted biomedicine. We are pleased to invite authors to submit reviews and original research articles in this exciting field to discuss their contributions and provide critical views on current mitochondrial research in modern biomedicines for therapeutic aims.

Dr. Paresh Prajapati
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 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. Biomedicines 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 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
  • mitochondrial diseases
  • mitochondrial therapy
  • mitophagy
  • pharmacology
  • therapeutic targeting
  • mitochondria
  • mtDNA
  • medical science
  • signaling
  • gene expression
  • mitochondrial dynamics
  • immunity

Published Papers (2 papers)

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Research

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22 pages, 3443 KiB  
Article
Phenotypic Characterization of Male Tafazzin-Knockout Mice at 3, 6, and 12 Months of Age
by Michelle V. Tomczewski, John Z. Chan, Zurie E. Campbell, Douglas Strathdee and Robin E. Duncan
Biomedicines 2023, 11(2), 638; https://doi.org/10.3390/biomedicines11020638 - 20 Feb 2023
Cited by 2 | Viewed by 2225
Abstract
Barth syndrome (BTHS) is an X-linked mitochondrial disease caused by mutations in the gene encoding for tafazzin (TAZ), a key enzyme in the remodeling of cardiolipin. Mice with a germline deficiency in Taz have been generated (Taz-KO) but not [...] Read more.
Barth syndrome (BTHS) is an X-linked mitochondrial disease caused by mutations in the gene encoding for tafazzin (TAZ), a key enzyme in the remodeling of cardiolipin. Mice with a germline deficiency in Taz have been generated (Taz-KO) but not yet fully characterized. We performed physiological assessments of 3-, 6-, and 12-month-old male Taz-KO mice, including measures of perinatal survival, growth, lifespan, gross anatomy, whole-body energy and substrate metabolism, glucose homeostasis, and exercise capacity. Taz-KO mice displayed reduced viability, with lower-than-expected numbers of mice recorded at 4 weeks of age, and a shortened lifespan due to disease progression. At all ages, Taz-KO mice had lower body weights compared with wild-type (Wt) littermates despite similar absolute food intakes. This finding was attributed to reduced adiposity and diminutive organs and tissues, including heart and skeletal muscles. Although there were no differences in basal levels of locomotion between age-matched genotypes, indirect calorimetry studies showed higher energy expenditure measures and respiratory exchange ratios in Taz-KO mice. At the youngest age, Taz-KO mice had comparable glucose tolerance and insulin action to Wt mice, but while these measures indicated metabolic impairments in Wt mice with advancing age that were likely associated with increasing adiposity, Taz-KO mice were protected. Comparisons across the three age-cohorts revealed a significant and more severe deterioration of exercise capacity in Taz-KO mice than in their Wt littermate controls. The Taz-KO mouse model faithfully recapitulates important aspects of BTHS, and thus provides an important new tool to investigate pathophysiological mechanisms and potential therapies. Full article
(This article belongs to the Special Issue Mitochondrial Function in Biomedicines)
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Review

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29 pages, 480 KiB  
Review
Mitochondrial Dysfunction in Cardiac Diseases and Therapeutic Strategies
by Yafei Huang and Bingying Zhou
Biomedicines 2023, 11(5), 1500; https://doi.org/10.3390/biomedicines11051500 - 22 May 2023
Cited by 9 | Viewed by 2260
Abstract
Mitochondria are the main site of intracellular synthesis of ATP, which provides energy for various physiological activities of the cell. Cardiomyocytes have a high density of mitochondria and mitochondrial damage is present in a variety of cardiovascular diseases. In this paper, we describe [...] Read more.
Mitochondria are the main site of intracellular synthesis of ATP, which provides energy for various physiological activities of the cell. Cardiomyocytes have a high density of mitochondria and mitochondrial damage is present in a variety of cardiovascular diseases. In this paper, we describe mitochondrial damage in mitochondrial cardiomyopathy, congenital heart disease, coronary heart disease, myocardial ischemia–reperfusion injury, heart failure, and drug-induced cardiotoxicity, in the context of the key roles of mitochondria in cardiac development and homeostasis. Finally, we discuss the main current therapeutic strategies aimed at alleviating mitochondrial impairment-related cardiac dysfunction, including pharmacological strategies, gene therapy, mitochondrial replacement therapy, and mitochondrial transplantation. It is hoped that this will provide new ideas for the treatment of cardiovascular diseases. Full article
(This article belongs to the Special Issue Mitochondrial Function in Biomedicines)
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