Evidence map›Paper›PMID 42850634›Full record

ReviewAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2026

Lactate Signal: Modulator of Cellular Energy Production and Anabolism.

Han Wang, Si-Yuan Yang, Wei Xu

Abstract readReview
PubMed Publisher
In one paragraph

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.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors.

Han WangThe Obstetrics & Gynecology Hospital of Fudan University, Shanghai Key Lab of Reproduction and Development, Shanghai Key Lab of Female Reproductive Endocrine Related Diseases, Shanghai Key Laboratory of Metabolic Remodeling and Health, Institute of Metabolism and Integrative Biology and State Key Laboratory of Genetics and Development of Complex Phenotypes, Fudan University, Shanghai, People's Republic of China.ORCID https://orcid.org/0000-0002-1442-4539
Si-Yuan YangThe Obstetrics & Gynecology Hospital of Fudan University, Shanghai Key Lab of Reproduction and Development, Shanghai Key Lab of Female Reproductive Endocrine Related Diseases, Shanghai Key Laboratory of Metabolic Remodeling and Health, Institute of Metabolism and Integrative Biology and State Key Laboratory of Genetics and Development of Complex Phenotypes, Fudan University, Shanghai, People's Republic of China.
Wei XuThe Obstetrics & Gynecology Hospital of Fudan University, Shanghai Key Lab of Reproduction and Development, Shanghai Key Lab of Female Reproductive Endocrine Related Diseases, Shanghai Key Laboratory of Metabolic Remodeling and Health, Institute of Metabolism and Integrative Biology and State Key Laboratory of Genetics and Development of Complex Phenotypes, Fudan University, Shanghai, People's Republic of China.ORCID https://orcid.org/0000-0002-9858-589X

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

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

anabolismcatabolismcell biologyglycolysislactate/pyruvatemetabolic pathwaysignal transduction

Identifiers

PMID42850634

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.