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Biomedicines
Special Issues
Mitochondrial Bioenergetics: From Cellular Metabolism to Therapeutic Target
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Mitochondrial Bioenergetics: From Cellular Metabolism to Therapeutic Target

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 August 2023) | Viewed by 8625

Special Issue Editor

Dr. Wei-Shiung Lian

E-Mail Website
Guest Editor
1. Core Laboratory for Phenomics and Diagnostic, Department of Medical Research, Chang Gung University College of Medicine, Kaohsiung Chang Gung Memorial Hospital, Kaohsiung 83301, Taiwan
2. Center for Mitochondrial Research and Medicine, Kaohsiung Chang Gung Memorial Hospital, Kaohsiung 83301, Taiwan
Interests: mitochondrial biology; osteoarthritis; osteoporosis; stem cells; cartilage biology; gut microbiota

Special Issue Information

Dear Colleagues,

This Special Issue, “Mitochondrial bioenergetics: from cellular metabolism to therapeutic target”, is now open for submissions. We sincerely invite you to participate.

This Special Issue will primarily focus on mitochondrial biology and bioenergetic function, which are implicated in the homeostasis of cellular metabolism and chronic disease pathogenesis. The discoveries and developments stemming from these studies will be extended to provide future research directions for disease treatment strategies. Mitochondria play a vital role in many biological systems that significantly adjust ATP synthase, adapt to cellular stress or lead to multiple diseases. Furthermore, the complex mitochondrial bioenergetic machinery correlates with the oxidative phosphorylation system (OXPHOS), which displays high flexibility to allow the remodeling of mitochondrial capacity to fulfill cellular elements. With the improvement of next-generation sequencing instruments and the advancement of bioinformatic analysis, there has been a great deal of emerging evidence of chronic diseases representing mitochondrial metabolism, ultrastructural integrity, microbiota metabolites targeting mitochondria, tRNA relative congenital disease, etc.

We are excited to provide scientists with a forum for the discussion of this topic, particularly those interested in topics that can expand the horizons of biomedicine and turn potential therapeutic research into strategies for clinical applications. We encourage authors in this field to submit original research or review articles on this critical and rapidly evolving field of biomedicine.

Dr. Wei-Shiung Lian
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

  • congenital disease
  • senescence
  • mitochondrial bioenergetics
  • microbiota metabolites
  • autophagy
  • mitophagy

Published Papers (3 papers)

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Research

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17 pages, 6704 KiB  
Article
COX5B-Mediated Bioenergetic Alterations Modulate Cell Growth and Anticancer Drug Susceptibility by Orchestrating Claudin-2 Expression in Colorectal Cancers
by Yu-De Chu, Siew-Na Lim, Chau-Ting Yeh and Wey-Ran Lin
Biomedicines 2022, 10(1), 60; https://doi.org/10.3390/biomedicines10010060 - 28 Dec 2021
Cited by 7 | Viewed by 1571
Abstract
Oxidative phosphorylation (OXPHOS) consists of four enzyme complexes and ATP synthase, and is crucial for maintaining physiological tissue and cell growth by supporting the main bioenergy pool. Cytochrome c oxidase (COX) has been implicated as a primary regulatory site of OXPHOS. Recently, COX [...] Read more.
Oxidative phosphorylation (OXPHOS) consists of four enzyme complexes and ATP synthase, and is crucial for maintaining physiological tissue and cell growth by supporting the main bioenergy pool. Cytochrome c oxidase (COX) has been implicated as a primary regulatory site of OXPHOS. Recently, COX subunit 5B (COX5B) emerged as a potential biomarker associated with unfavorable prognosis by modulating cell behaviors in specific cancer types. However, its molecular mechanism remains unclear, particularly in colorectal cancers (CRCs). To understand the role of COX5B in CRCs, the expression and postoperative outcome associations using independent in-house patient cohorts were evaluated. A higher COX5B tumor/nontumor expression ratio was associated with unfavorable clinical outcomes (p = 0.001 and 0.011 for overall and disease-free survival, respectively. In cell-based experiments, the silencing of COX5B repressed cell growth and enhanced the susceptibility of CRCs cells to anticancer drugs. Finally, downstream effectors identified by RNA sequencing followed by RT-qPCR and functional compensation experiments revealed that the tight junction protein Claudin-2 (CLDN2) acts downstream of COX5B-mediated bioenergetic alterations in controlling cell growth and the sensitivity to anticancer drugs in CRCs cells. In conclusion, it was found that COX5B promoted cell growth and attenuated anticancer drugs susceptibility in CRCs cells by orchestrating CLDN2 expression, which may contribute to unfavorable postoperative outcomes of patients with CRCs. Full article
(This article belongs to the Special Issue Mitochondrial Bioenergetics: From Cellular Metabolism to Therapeutic Target)
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Review

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18 pages, 686 KiB  
Review
The Potential Important Role of Mitochondrial Rieske Iron–Sulfur Protein as a Novel Therapeutic Target for Pulmonary Hypertension in Chronic Obstructive Pulmonary Disease
by Lillian Truong, Yun-Min Zheng and Yong-Xiao Wang
Biomedicines 2022, 10(5), 957; https://doi.org/10.3390/biomedicines10050957 - 21 Apr 2022
Cited by 1 | Viewed by 2128
Abstract
Chronic obstructive pulmonary disease (COPD) is the third leading cause of death worldwide, which is often due to pulmonary hypertension (PH). The underlying molecular mechanisms are poorly understood, and current medications are neither specific nor always effective. In this review, we highlight the [...] Read more.
Chronic obstructive pulmonary disease (COPD) is the third leading cause of death worldwide, which is often due to pulmonary hypertension (PH). The underlying molecular mechanisms are poorly understood, and current medications are neither specific nor always effective. In this review, we highlight the recent findings on the roles of altered mitochondrial bioenergetics in PH in COPD. We also discuss the central role of mitochondrial reactive oxygen species (ROS) generation mediated by Rieske iron–sulfur protein (RISP) and review the contributions of RISP-dependent DNA damage and NF-κB-associated inflammatory signaling. Finally, the potential importance of mitochondrial RISP and its associated molecules as novel therapeutic targets for PH in COPD are meticulously discussed. Full article
(This article belongs to the Special Issue Mitochondrial Bioenergetics: From Cellular Metabolism to Therapeutic Target)
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20 pages, 805 KiB  
Review
Gut Microbiota Ecosystem Governance of Host Inflammation, Mitochondrial Respiration and Skeletal Homeostasis
by Wei-Shiung Lian, Feng-Sheng Wang, Yu-Shan Chen, Ming-Hsien Tsai, How-Ran Chao, Holger Jahr, Re-Wen Wu and Jih-Yang Ko
Biomedicines 2022, 10(4), 860; https://doi.org/10.3390/biomedicines10040860 - 06 Apr 2022
Cited by 14 | Viewed by 4189
Abstract
Osteoporosis and osteoarthritis account for the leading causes of musculoskeletal dysfunction in older adults. Senescent chondrocyte overburden, inflammation, oxidative stress, subcellular organelle dysfunction, and genomic instability are prominent features of these age-mediated skeletal diseases. Age-related intestinal disorders and gut dysbiosis contribute to host [...] Read more.
Osteoporosis and osteoarthritis account for the leading causes of musculoskeletal dysfunction in older adults. Senescent chondrocyte overburden, inflammation, oxidative stress, subcellular organelle dysfunction, and genomic instability are prominent features of these age-mediated skeletal diseases. Age-related intestinal disorders and gut dysbiosis contribute to host tissue inflammation and oxidative stress by affecting host immune responses and cell metabolism. Dysregulation of gut microflora correlates with development of osteoarthritis and osteoporosis in humans and rodents. Intestinal microorganisms produce metabolites, including short-chain fatty acids, bile acids, trimethylamine N-oxide, and liposaccharides, affecting mitochondrial function, metabolism, biogenesis, autophagy, and redox reactions in chondrocytes and bone cells to regulate joint and bone tissue homeostasis. Modulating the abundance of Lactobacillus and Bifidobacterium, or the ratio of Firmicutes and Bacteroidetes, in the gut microenvironment by probiotics or fecal microbiota transplantation is advantageous to suppress age-induced chronic inflammation and oxidative damage in musculoskeletal tissue. Supplementation with gut microbiota-derived metabolites potentially slows down development of osteoarthritis and osteoporosis. This review provides latest molecular and cellular insights into the biological significance of gut microorganisms and primary and secondary metabolites important to cartilage and bone integrity. It further highlights treatment options with probiotics or metabolites for modulating the progression of these two common skeletal disorders. Full article
(This article belongs to the Special Issue Mitochondrial Bioenergetics: From Cellular Metabolism to Therapeutic Target)
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