ArticleJournal of advanced research2026
Elevated lactate production exacerbates PM2.5-induced pulmonary fibrosis by stabilizing TGF-β1.
Article in Journal of advanced research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- Lactate metabolism and protein lactylation in inflammatory and tumor microenvironments.Molecular biomedicine · 2026Review
- Hallmarks of lung cancer driven by inhalable particulate matter: From cell-intrinsic oncogenic traits to microenvironment remodeling.Innovation (Cambridge (Mass.)) · 2026Review
- Mechanistic Studies of Lactate in Heart Failure: From Metabolic Biomarker to Therapeutic Target.Reviews in cardiovascular medicine · 2026Review
- Metabolic reprogramming in fibrosis-related diseases: underlying mechanisms and therapeutics.Molecular biomedicine · 2026Review
- Glycolytic lactylation modulates cell death decisions in diabetic kidney disease: Metabolic‑epigenetic interplay between ferroptosis and autophagy in fibrotic remodeling (Review).International journal of molecular medicine · 2026Review
- Lactylation in tissue fibrosis: epigenetic mechanisms, metabolic crosstalk, and therapeutic opportunities.Journal of translational medicine · 2026Review
- Lactylation in pulmonary fibrosis: current understanding and challenges.Journal of translational medicine · 2026Review
- Mitochondrial PDHA1 acetylation orchestrates lactate-dependent epigenetic reprogramming to promote fibrosis via NUAK2.Cellular and molecular life sciences : CMLS · 2026Article
- Review
- Beyond a metabolite: lactate and lactylation in lung diseases.Respiratory research · 2026Review
- Lactylation Modification: From Basic Biological Process to Clinical Cardiovascular Diseases.Research (Washington, D.C.) · 2026Review
Corrections and comments
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Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionLactate, a glycolysis byproduct, has been implicated in the fibrotic process, while transforming growth factor-beta 1 (TGF-β1) plays a central role in promoting fibrosis. Air pollution, particularly fine particulate matter (PM2.5), represents a significant environmental risk factor for the development of pulmonary fibrosis. However, the role of lactate and the underlying mechanisms by which it acts in PM2.5-induced pulmonary fibrosis remain poorly understood.
objectivesThis study aimed to identify the cell types contributing to lactate accumulation in lung tissue during PM2.5-induced pulmonary fibrosis and elucidate the mechanism by which lactate regulates TGF-β1.
methodsSeven types of lung cells from PM2.5-exposed mice were isolated using fluorescence-activated cell sorting to determine their lactate production. Immunoprecipitation and immunoblotting were performed to assess the impact of lactate on TGF-β1 stability. The effect of histone lactylation on Stub1 gene expression was investigated by chromatin immunoprecipitation assays.
resultsMacrophages exhibited elevated lactate production during PM2.5-induced pulmonary fibrosis. Elevated intracellular lactate levels in macrophages suppressed the expression of carboxyl terminus of Hsc70-interacting protein (CHIP, encoded by Stub1) via the enrichment of lactylated H3K18 at the Stub1 promoter locus. Consequently, reduced CHIP expression impeded TGF-β1 degradation, promoted enhanced TGF-β1 secretion by macrophages, and exacerbated pulmonary fibrosis symptoms. Moreover, the inhibition of lactate production significantly alleviated the pulmonary fibrosis phenotype in PM2.5-exposed mice.
conclusionElevated lactate production in macrophages induced by PM2.5 inhibits the ubiquitination and degradation of TGF-β1 through the suppression of CHIP expression, thereby enhancing TGF-β1 secretion and exacerbating pulmonary fibrosis.
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