Editorial: Immunometabolism at the intersection of signaling networks and therapeutic strategies
Year: 2026
Type: editorial
Abstract: Immunometabolism at the intersection of signaling networks and therapeutic strategiesThis Research Topic highlights recent advances in the molecular and cellular mechanisms underlying metabolic-immune crosstalk across aging, inflammation, obesity, cancer, and neurological disease.Collectively, the studies demonstrate how metabolic pathways and their regulatory metabolites shape innate and adaptive immune function by integrating cellular bioenergetics with signaling, stress responses, and tissue-specific cues.In this context, the identification of key metabolic regulators and metabolites provides important insights into the mechanisms governing immune-cell adaptation and inflammatory responses.Furthermore, the papers published under this Research Topic emphasize metabolic remodeling as a potential therapeutic target, supporting the development of strategies to selectively modulate immune function across diverse pathological settings.Recent studies have expanded our understanding of the interplay between mitochondrial homeostasis, immune function, and aging, highlighting complementary mechanisms through which mitochondrial quality control and metabolic adaptation shape immune responses.Ferreira et al. reviewed key mitochondrial proteases, including CLPXP, LONP1, m-AAA, i-AAA/YME1L, and OMA1, emphasizing that their functions extend beyond the removal of damaged proteins to include the regulation of mitochondrial dynamics, ROS production, cellular stress signaling, and mitochondria-derived danger signals, thereby modulating immune responses in a context-dependent manner.Similarly, Lewis et al. proposed that effective adaptation to mitochondrial stress through the mitochondrial unfolded protein response (mtUPR) is important for maintaining T reg metabolic fitness and suppressive function during aging.Consistent with this framework, Queiroz et al. demonstrated in senescence-accelerated SAMP8 and senescence-resistant SAMR1 mice that metabolic and mitochondrial pathways can be pharmacologically modulated during aging. Six months of intermittent low-dose rapamycin increased hepatic mitochondrial respiratoryFrontiers in Immunology frontiersin.
Source: Frontiers in Immunology
Institutions: Universidade de São Paulo, Trinity College Dublin
Language: English
Topic: Immune cells in cancer
Subfield: Immunology
Field: Immunology and Microbiology
Domain: Life Sciences
Open Access status: gold
Estimated APC paid: $3,801
OpenAlex ID: W7220656826