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Mitochondrial Medicine: Pharmacological Targeting of Mitochondria in Disease—2nd Edition

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pharmacology".

Deadline for manuscript submissions: closed (20 March 2025) | Viewed by 2003

Special Issue Editors


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Dipartimento di Scienze Biotecnologiche di Base, Cliniche Intensivologiche e Perioperatorie, Università Cattolica del Sacro Cuore, Largo Francesco Vito 1, 00168 Rome, Italy
Interests: cell differentiation; cancer; cancer cell metabolism; mitochondria; mitochondrial metabolism; oxidative phosphorylation; tumor markers; Warburg effect
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Special Issue Information

Dear Colleagues,

This is a continued series of the hot topic of Mitochondrial Medicine: Pharmacological Targeting of Mitochondria in Disease; our first Special Issue of this topic received interesting contributions and discussions (https://www.mdpi.com/journal/ijms/special_issues/Mitochondrial_Medicine).

Mitochondria are fundamental organelles in cell biology. They can no longer be considered simply the powerhouse of the cell because this fundamental function is strictly related to different activities of the cell (apoptosis, signal transduction, thermogenesis, proliferation, differentiation, and so on). Experimental research gives some light to molecular mechanisms at the basis of these complex and interconnected functions with significant advances in knowledge of the etiopathogenesis, pathophysiology, and therapeutic approaches of different diseases. Importantly, these different pathologies are not limited to typical mitochondrial disorders but affect a wide range of acute and chronic diseases (i.e., ischemic disorders, infectious diseases, neurodegenerative diseases, infertility, psychotic disorder, dermopathies, sepsis, and above all, cancer). The growing pathophysiological role of mitochondria is further demonstrated by the number of clinical studies, recorded by ClinicalTrials.gov, showing mitochondria in their keywords panel (at present, more than 1500 clinical studies).

To date, the pharmacology of mitochondria includes molecules which can enrich the NAD+ pool and/or “stimulate” oxidative metabolism (i.e., carnitine), molecules that protect these organelles by the end products of their oxidative metabolism (i.e., Q10, mitoQ, dicumarols and son on); however, some interesting new drugs are now under evaluation.

Last but not least, some intriguing parmacotoxicological aspects, too often neglected, on mitochondria, as innocent bystanders, are well-known (fibrates, statins, reverse-transcriptase inhibitors). All these data further push to deepen our understanding of and promote such a fascinating, innovative, and promising therapeutic approach.

This Special Issue focuses on the research field of the pharmacology of mitochondria; Original research articles, short communications, and reviews, both narrative and systematic, are all welcome for submission to this Special Issue.

Dr. Patrizia Bottoni
Prof. Dr. Roberto Scatena
Guest Editors

Manuscript Submission Information

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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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

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Keywords

  • cancer
  • complex I (NADH: ubiquinone oxidoreductase)
  • drug toxicity
  • mitochondria
  • reactive oxygen species (ROS)
  • therapeutic drug monitoring
  • cancer stem cells
  • cancer cell differentiation
  • cancer cell metabolism
  • cancer diagnosis
  • cancer therapy
  • complex I
  • oxidative phoshorylation
  • tumor markers
  • Warburg effect

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Published Papers (1 paper)

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Research

15 pages, 15159 KiB  
Article
Apoptosis, Mitochondrial Autophagy, Fission, and Fusion Maintain Mitochondrial Homeostasis in Mouse Liver Under Tail Suspension Conditions
by Lu-Fan Li, Jiao Yu, Rui Li, Shan-Shan Li, Jun-Yao Huang, Ming-Di Wang, Li-Na Jiang, Jin-Hui Xu and Zhe Wang
Int. J. Mol. Sci. 2024, 25(20), 11196; https://doi.org/10.3390/ijms252011196 - 18 Oct 2024
Viewed by 1489
Abstract
Microgravity can induce alterations in liver morphology, structure, and function, with mitochondria playing an important role in these changes. Tail suspension (TS) is a well-established model for simulating the effects of microgravity on muscles and bones, but its impact on liver function remains [...] Read more.
Microgravity can induce alterations in liver morphology, structure, and function, with mitochondria playing an important role in these changes. Tail suspension (TS) is a well-established model for simulating the effects of microgravity on muscles and bones, but its impact on liver function remains unclear. In the current study, we explored the regulatory mechanisms of apoptosis, autophagy, fission, and fusion in maintaining liver mitochondrial homeostasis in mice subjected to TS for 2 or 4 weeks (TS2 and TS4). The results showed the following: (1) No significant differences were observed in nuclear ultrastructure or DNA fragmentation between the control and TS-treated groups. (2) No significant differences were detected in the mitochondrial area ratio among the three groups. (3) Cysteine aspartic acid-specific protease 3 (Caspase3) activity and the Bcl-2-associated X protein (bax)/B-cell lymphoma-2 (bcl2) ratio were not higher in the TS2 and TS4 groups compared to the control group. (4) dynamin-related protein 1 (DRP1) protein expression was increased, while mitochondrial fission factor (MFF) protein levels were decreased in the TS2 and TS4 groups compared to the control, suggesting stable mitochondrial fission. (5) No significant differences were observed in the optic atrophy 1 (OPA1), mitofusin 1 and 2 (MFN1 and MFN2) protein expression levels across the three groups. (6) Mitochondrial autophagy vesicles were present in the TS2 and TS4 groups, with a significant increase in Parkin phosphorylation corresponding to the duration of the TS treatment. (7) ATP synthase and citrate synthase activities were significantly elevated in the TS2 group compared to the control group but were significantly reduced in the TS4 group compared to the TS2 group. In summary, the coordinated regulation of apoptosis, mitochondrial fission and fusion, and particularly mitochondrial autophagy preserved mitochondrial morphology and contributed to the restoration of the activities of these two key mitochondrial enzymes, thereby maintaining liver mitochondrial homeostasis in mice under TS conditions. Full article
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