ReviewJournal of experimental & clinical cancer research : CR2022
Mitochondria dysfunction in CD8+ T cells as an important contributing factor for cancer development and a potential target for cancer treatment: a review.
Review in Journal of experimental & clinical cancer research : CR, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
63 citing papers in PubMed, 89 citations in OpenAlex.
- Article
- A Dosimetric Reappraisal of the Photobiomodulation Literature Assessing Animal Safety and Phototoxicity Evidence for Photobiomodulation in Oncology: Phantom Dangers.Biomedicines · 2026Review
- Review
- β-Adrenergic receptors as immunomodulators in T cells: mechanisms of neuroimmune crosstalk and pathophysiological implications.Molecular medicine (Cambridge, Mass.) · 2026Review
- Mitochondrial transfer between tumor and immune cells: a nexus of metabolic adaptation and immune dysfunction.Biomarker research · 2026Review
- T Cell Exhaustion in Cancer Immunotherapy: Heterogeneity, Mechanisms, and Therapeutic Opportunities.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- CD8Nature reviews. Cardiology · 2026Review
- Heart-homed nanomedicine induces fast mitochondrial rescue to enhance cardiac function post-myocardial infarction.Bioactive materials · 2026Article
- Machine learning-driven identification of shared and disease-specific mitochondria-related genes in COPD, NSCLC, and NSCLC with COPD.iScience · 2026Article
- Molecular pixelation of the CAR T cell surface proteome.bioRxiv : the preprint server for biology · 2026Article
- Balancing Intrinsic and Extrinsic Factors in CD8Immune network · 2026Review
- Light Metabolically Reprograms CD8Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Single-cell and pseudobulk analyses reveal hidden mitochondrial expression imbalance in gastric cancer.Frontiers in genetics · 2026Article
- Mitochondria-Targeted Nanoformulations: New Therapeutic Strategies and Opportunities for Cancer Immunotherapy.Current drug targets · 2026Review
- Loss of SETD2-mediated H3K36me3 Drives CD8Research (Washington, D.C.) · 2026Article
- Mannose and phenylboronate ester functionalized mesoporous silica nanoparticles contained in chitosan microneedles for enhancing cellular immunity and antitumor efficacy.Theranostics · 2026Article
- Harnessing Machine Learning and Multiomics to Construct a Tumor-Specific T Cell Signature for Prognostic Assessment and Precision Medicine in Lung Adenocarcinoma.Annals of surgical oncology · 2026Article
- A smart amphiphilic nanoplatform amplifies ROS-mediated immunogenic cell death to suppress bladder cancer growth and metastasis.Journal of nanobiotechnology · 2025Article
- Ubiquitous Expression ofLife (Basel, Switzerland) · 2025Article
- The Role and Research Progress of CD8Biomedicines · 2025Review
3 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 4 institutions in 1 country.
Funding
Abstract
CD8+ T cells play a central role in anti-tumor immunity. Naïve CD8+ T cells are active upon tumor antigen stimulation, and then differentiate into functional cells and migrate towards the tumor sites. Activated CD8+ T cells can directly destroy tumor cells by releasing perforin and granzymes and inducing apoptosis mediated by the death ligand/death receptor. They also secrete cytokines to regulate the immune system against tumor cells. Mitochondria are the central hub of metabolism and signaling, required for polarization, and migration of CD8+ T cells. Many studies have demonstrated that mitochondrial dysfunction impairs the anti-tumor activity of CD8+ T cells through various pathways. Mitochondrial energy metabolism maladjustment will cause a cellular energy crisis in CD8+ T cells. Abnormally high levels of mitochondrial reactive oxygen species will damage the integrity and architecture of biofilms of CD8+ T cells. Disordered mitochondrial dynamics will affect the mitochondrial number and localization within cells, further affecting the function of CD8+ T cells. Increased mitochondria-mediated intrinsic apoptosis will decrease the lifespan and quantity of CD8+ T cells. Excessively low mitochondrial membrane potential will cause the release of cytochrome c and apoptosis of CD8+ T cells, while excessively high will exacerbate oxidative stress. Dysregulation of mitochondrial Ca2+ signaling will affect various physiological pathways in CD8+ T cells. To some extent, mitochondrial abnormality in CD8+ T cells contributes to cancer development. So far, targeting mitochondrial energy metabolism, mitochondrial dynamics, mitochondria-mediated cell apoptosis, and other mitochondrial physiological processes to rebuild the anti-tumor function of CD8+ T cells has proved effective in some cancer models. Thus, mitochondria in CD8+ T cells may be a potential and powerful target for cancer treatment in the future.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.