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Cells
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Mitochondrial Biology and Pathophysiology
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Mitochondrial Biology and Pathophysiology

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Pathology".

Deadline for manuscript submissions: 31 December 2024 | Viewed by 1216

Special Issue Editors

Prof. Dr. José M. Cuezva

E-Mail Website
Guest Editor
Centro de Biología Molecular Severo Ochoa (CBMSO, Consejo Superior de Investigaciones Científicas-Universidad Autónoma de Madrid), Madrid, Spain
Interests: mitochondria; ATP synthase; ATPase inhibitory factor 1; cancer; ageing; biomarkers; oxidative stress
Prof. Dr. Laura Formentini

E-Mail Website
Guest Editor
Departamento de Biología Molecular, Instituto Universitario de Biología Molecular IUBM, Centro de Biología Molecular Severo Ochoa (CBMSO, Consejo Superior de Investigaciones Científicas-Universidad Autónoma de Madrid), Universidad Autónoma de Madrid, Madrid, Spain
Interests: mitochondria; lipid metabolism; beta-oxidation; OXPHOS; bioenergetics; coenzyme Q; oxidative stress; ageing; metabolic disorders.

Special Issue Information

Dear Colleagues,

Mitochondria are highly dynamic and responsive organelles that regulate a variety of cellular functions and dictate cell fate. They play pivotal roles in orchestrating cellular signaling and differentiation, as well as in regulating oxidative stress, redox pathways, metabolism, aging, cell death, and immunomodulation. Hence, mitochondrial dysfunction is associated with many pathological conditions, such as cancer, cardiovascular diseases, metabolic syndrome, neurodegenerative diseases, and age-related disorders. Therefore, mitochondria are considered to be important therapeutic targets for these highly prevalent pathologies. However, the molecular mechanisms associated with the pathogenic progression of mitochondrial dysfunction remain to unidentified.

This Special Issue will focus on mitochondrial biology and pathophysiology and aims to collect original research articles or review articles from scholars in the field.

We look forward to receiving your manuscripts.

Prof. Dr. José M. Cuezva
Prof. Dr. Laura Formentini
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. Cells 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
  • age-related diseases
  • animal models
  • cell death
  • immune responses
  • metabolic responses
  • mitochondrial structure
  • dynamics and function proteostasis

Published Papers (1 paper)

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Research

17 pages, 4939 KiB  
Article
Inhibitors of Rho/MRTF/SRF Transcription Pathway Regulate Mitochondrial Function
by Pankaj Patyal, Xiaomin Zhang, Ambika Verma, Gohar Azhar and Jeanne Y. Wei
Cells 2024, 13(5), 392; https://doi.org/10.3390/cells13050392 - 24 Feb 2024
Viewed by 894
Abstract
RhoA-regulated gene transcription by serum response factor (SRF) and its transcriptional cofactor myocardin-related transcription factors (MRTFs) signaling pathway has emerged as a promising therapeutic target for pharmacological intervention in multiple diseases. Altered mitochondrial metabolism is one of the major hallmarks of cancer, therefore, [...] Read more.
RhoA-regulated gene transcription by serum response factor (SRF) and its transcriptional cofactor myocardin-related transcription factors (MRTFs) signaling pathway has emerged as a promising therapeutic target for pharmacological intervention in multiple diseases. Altered mitochondrial metabolism is one of the major hallmarks of cancer, therefore, this upregulation is a vulnerability that can be targeted with Rho/MRTF/SRF inhibitors. Recent advances identified a novel series of oxadiazole-thioether compounds that disrupt the SRF transcription, however, the direct molecular target of these compounds is unclear. Herein, we demonstrate the Rho/MRTF/SRF inhibition mechanism of CCG-203971 and CCG-232601 in normal cell lines of human lung fibroblasts and mouse myoblasts. Further studies investigated the role of these molecules in targeting mitochondrial function. We have shown that these molecules hyperacetylate histone H4K12 and H4K16 and regulate the genes involved in mitochondrial function and dynamics. These small molecule inhibitors regulate mitochondrial function as a compensatory mechanism by repressing oxidative phosphorylation and increasing glycolysis. Our data suggest that these CCG molecules are effective in inhibiting all the complexes of mitochondrial electron transport chains and further inducing oxidative stress. Therefore, our present findings highlight the therapeutic potential of CCG-203971 and CCG-232601, which may prove to be a promising approach to target aberrant bioenergetics. Full article
(This article belongs to the Special Issue Mitochondrial Biology and Pathophysiology)
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