Mitochondria: Multifaceted Regulators of Cell Death

A Special Issue of Cells (ISSN 2073-4409).

Deadline for manuscript submissions: 10 October 2026 | Viewed by 1226

Editors


E-Mail Website
Guest Editor
Laboratory of Biochemistry, Neuroscience Institute, Lithuanian University of Health Sciences, Kaunas, Lithuania
Interests: mitochondria; cardiolipin oxidation

E-Mail Website
Guest Editor
Laboratory of Biochemistry, Neuroscience Institute, Lithuanian University of Health Sciences, Kaunas, Lithuania
Interests: chemical and natural substances; heart and liver mitochondria

Special Issue Information

Dear Colleagues,

Mitochondria are intracellular organelles that are involved in energy production, cell metabolism, and cell signaling and consume over 95% of all oxygen that reaches our cells in order to produce ATP through oxidative phosphorylation. Mitochondria are essential not only in the process of energetic ATP synthesis but also in lipid metabolism, amino acid metabolism, the TCA cycle, and nucleic acid metabolism. Moreover, mitochondria play critical roles in many physiological processes, such as redox or calcium homeostasis, and produce large amounts of reactive oxygen species (ROS), which serve as signaling molecules but also cause oxidative damage. Excessive amount of ROS can trigger cell death by damaging mitochondrial DNA, lipids, and proteins. Mitochondria are multifaceted regulators of cell death, acting through the release of factors, controlling ROS levels, maintaining membrane integrity, and modulating interactions with other cell components.

Mitochondria can act as signaling molecules and are transferred between cells, influencing cellular function and potentially playing a role in disease. This intercellular mitochondrial transfer involves the movement of whole mitochondria from one cell to another (tunneling nanotubes, extracellular vesicles), either to enhance cellular function in recipient cells or to aid in the removal of dysfunctional mitochondria. Mitochondrial transfer can also involve the transfer of mitochondrial DNA (mtDNA), which can have implications for the recipient cell's function. Healthy mitochondria can be transferred to cells with damaged mitochondria, potentially restoring function. Mitochondrial transfer is emerging as a potential target for cancer treatment and hindering cancer progression. Transferring healthy mitochondria into cancer cells can make them more susceptible to chemotherapy and radiation therapy.

Dr. Rasa Banienė
Dr. Sonata Trumbeckaite
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 communications are invited. For planned papers, a title and short abstract (about 250 words) can be sent to the Editorial Office for assessment.

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-anonymized 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
  • cell death
  • multifaceted regulators
  • reactive oxygen species (ROS)
  • cell metabolism
  • mitochondrial transfer

Benefits of Publishing in a Special Issue

  • Ease of navigation: Grouping papers by topic helps scholars navigate broad scope journals more efficiently.
  • Greater discoverability: Special Issues support the reach and impact of scientific research. Articles in Special Issues are more discoverable and cited more frequently.
  • Expansion of research network: Special Issues facilitate connections among authors, fostering scientific collaborations.
  • External promotion: Articles in Special Issues are often promoted through the journal's social media, increasing their visibility.
  • Reprint: MDPI Books provides the opportunity to republish successful Special Issues in book format, both online and in print.

Further information on MDPI's Special Issue policies can be found here.

Published Papers (1 paper)

Order results
Result details
Select all
Export citation of selected articles as:

Review

25 pages, 1782 KB  
Review
The Interplay of Splicing and Metabolism in Cancer
by Dillon M. Voss, Yange Cui and Peter S. Klein
Cells 2026, 15(12), 1117; https://doi.org/10.3390/cells15121117 - 20 Jun 2026
Viewed by 631
Abstract
Aberrant RNA splicing and metabolic reprogramming are defining hallmarks of cancer that were historically studied as parallel processes. Increasing evidence now reveals extensive crosstalk between these pathways, whereby RNA splicing reshapes metabolic circuits, and metabolic states reciprocally influence splice-site selection and spliceosome activity. [...] Read more.
Aberrant RNA splicing and metabolic reprogramming are defining hallmarks of cancer that were historically studied as parallel processes. Increasing evidence now reveals extensive crosstalk between these pathways, whereby RNA splicing reshapes metabolic circuits, and metabolic states reciprocally influence splice-site selection and spliceosome activity. In this review, we synthesize recent mechanistic insights into how splicing programs regulate metabolic adaptation across diverse cancer contexts. We discuss recurrent oncogenic mutations in spliceosomal components and dysregulation of RNA-binding proteins (RBPs) that drive alternative splicing events in key metabolic regulators, which promote metabolic plasticity required for tumor growth. We further examine how metabolites and nutrient-sensing pathways directly modulate splicing factor activity, spliceosome dynamics, and RNA processing. We also summarize a new mechanism of mitochondrial quality control mediated by retrograde signals from mitochondria to the spliceosome to enhance mitophagy of dysfunctional mitochondria. Full article
(This article belongs to the Special Issue Mitochondria: Multifaceted Regulators of Cell Death)
Show Figures

Figure 1

Back to TopTop