ArticleJournal of clinical laboratory analysis2025
Inhibition of Lactate Accumulation via USP38-Mediated MCT1 Deubiquitination Activates AKT/mTOR Signaling to Mitigate PM2.5-Induced Lung Injury.
Article in Journal of clinical laboratory analysis, 2025. 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
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.
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
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
Abstract
backgroundLactate, traditionally viewed as a glycolysis byproduct, has emerged as an important mediator influencing immunity, inflammation, and tissue damage. While PM2.5 exposure is known to cause various metabolic disturbances, the role of lactate metabolism in PM2.5-induced lung injury remains unclear. This study aims to elucidate the mechanisms underlying PM2.5-induced lung injury from a metabolic perspective.
methodsLactate and pyruvate assays were performed to assess metabolic changes following PM2.5 exposure. Protein expression and tissue damage were assessed using Western blot, IHC, ELISA, and TUNEL staining. The biological role of USP38 in PM2.5-induced injury was identified using gain- and loss-of-function experiments. Co-immunoprecipitation and ubiquitination assays were conducted to analyze the interaction between USP38 and MCT1, as well as the regulation of MCT1 deubiquitination. The role of MCT1 in lactate metabolism and PM2.5-induced apoptosis was validated through gene editing. Proteomics revealed the potential mechanisms involved in USP38 regulation of apoptosis.
resultsOur results demonstrated that PM2.5 exposure induced lactate accumulation, leading to cell apoptosis and lung injury. USP38 stabilized MCT1 expression by deubiquitination, facilitating lactate export and reducing apoptosis and lung injury caused by lactate accumulation. Mechanistically, PM2.5 increased lactate production, suppressed AKT/mTOR pathway activation, and promoted apoptosis and lung injury. USP38 promoted lactate export through MCT1, activated the AKT/mTOR pathway, and mitigated PM2.5-induced lung injury.
conclusionUSP38 reduces lactate accumulation by promoting AKT/mTOR pathway activation through MCT1-mediated lactate export, thereby alleviating PM2.5-induced lung injury. These findings reveal a novel mechanism of PM2.5-related lung injury and highlight potential therapeutic targets.
Indexed as
Identifiers
What 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.