ReviewAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2026
Lactate Signal: Modulator of Cellular Energy Production and Anabolism.
Review in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
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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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lactate is no longer viewed simply as a glycolytic end-product, but as a compartmentalized signaling metabolite that coordinates energy production, carbon redistribution, redox balance, and anabolic commitment. This review discusses lactate as a regulator of the catabolism-anabolism axis, emphasizing two major patterns of molecular interpretation. First, lactate acts through non-covalent mechanisms, including transporter-mediated flux, receptor-dependent sensing, pH-linked effects, and direct binding to intracellular proteins. These processes allow lactate-rich states to rapidly couple metabolic flux to signaling pathways. Second, lactate-associated metabolic states are translated into the dynamic and reversible change of covalent post-translational modifications, including histone and non-histone lactylation. Histone lactylation connects glycolytic metabolism to transcriptional regulation, whereas non-histone lactylation expands lactate-dependent control to immune signaling, mitochondrial metabolism, DNA repair, cardiovascular stress, tissue remodeling, and cancer progression. We further discuss how extracellular, cytosolic, mitochondrial-associated, and nuclear lactate pools provide distinct biochemical contexts in which lactate-dependent mechanisms can operate. By integrating lactate transport, receptor sensing, protein binding, metabolism, and lactylation, this Review uses compartmental organization as a framework for synthesizing how lactate-rich states influence metabolic adaptation, stress responses, immune regulation, tissue remodeling, disease progression, and, in selected contexts, anabolic or reparative programs.
Indexed as
Identifiers
42850634What OpenQuestion holds
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.