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Metabolic Signalling in Cell Fate, Tissue Homeostasis, and Disease

Metabolic signalling has emerged as a master regulator of virtually every cell biological process, from proliferation and differentiation to senescence and death. Nutrients are not merely fuel; they are signalling molecules. mTORC1 integrates amino acid and energy status to gate anabolic programmes. AMPK acts as a low-energy sentinel. Acetyl-CoA, NAD⁺, α-ketoglutarate, and succinate directly feed into epigenetic remodelling. HIF-1α rewires transcription under oxygen and glucose stress. Together these pathways form a metabolic signalling network that cells use to read their environment and commit to a fate.This Research Topic invites original research, reviews, and perspectives on how metabolic signals are sensed, transduced, and decoded to control cell and tissue behaviour, and how their dysregulation drives disease.SubtopicsNutrient sensing hubs - mTORC1/2, AMPK, LKB1, and their upstream sensorsMetabolite signalling - acetyl-CoA, NAD⁺/NADH, α-KG, succinate, and itaconate as second messengersMetabolic control of epigenetics - how metabolic flux shapes the chromatin landscapeLipid and lipid-derived signals - ceramides, eicosanoids, lysophospholipids, and fatty acid sensingAmino acid signalling - leucine, glutamine, arginine sensing and downstream effectorsHIF and oxygen sensing - PHD–HIF axis, pseudohypoxia, and metabolic rewiringMitochondria as signalling organelles - ROS, mtDNA, cristae dynamics, and retrograde signallingMetabolic regulation of cell fate - proliferation, quiescence, differentiation, and senescenceInter-organ metabolic crosstalk - hormones, exosomes, and metabolites as systemic signalsMetabolic signalling in disease - cancer, diabetes, neurodegeneration, and cardiovascular diseaseMetabolic regulation of cell function Topic editors: María Gracia Gervasi, Xingzhou Peng, Ronghui Li, Maria Teresa Bengoechea Alonso Source: https://www.frontiersin.org/research-topics/82433/metabolic-signalling-in-cell-fate-tissue-homeostasis-and-disease

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