Mitochondrial Energy Metabolism in Cancer, Immunoregulation and Antitumour Response.
Level 5 - mechanism / opinion, no new human data
Narrative review describing biological mechanisms without primary human data or systematic review methodology.
PubMed 42435181 · doi:10.1007/978-3-032-12166-0_17
What was done
This narrative review synthesizes literature on the roles of mitochondrial energy metabolism and extra-metabolic signaling in cancer progression, immune cell regulation, and antitumor responses. It examines bioenergetic reprogramming—including oxidative phosphorylation, glycolysis, tricarboxylic acid cycle remodeling, and redox balance—as well as mitochondrial signaling mediators (reactive oxygen species, lactate shuttling, mitochondrial DNA release) and their therapeutic relevance to cancer immunotherapies such as checkpoint inhibitors, adoptive T-cell transfer, and natural killer cell therapies.
What was found
The abstract provides qualitative mechanistic descriptions and reports no quantitative data, effect sizes, or study counts. It details how mitochondrial metabolic plasticity and retrograde signaling molecules modulate innate and adaptive immune responses within the tumor microenvironment to support tumor immune evasion.
Why it matters
It maps conceptual mechanisms connecting mitochondrial metabolism to immune evasion, pointing to mitochondrial pathways as candidate targets to overcome immunosuppression in cancer immunotherapy.
Limits
The work is a narrative review chapter that lacks a systematic search protocol, quality assessment of cited studies, or quantitative meta-analysis. No novel empirical data, patient populations, or clinical outcomes are reported in the abstract.
Cited by
- contradicts All cancer cells ever examined have defects in the number, structure, and function of their mitochondria.