ReviewAnimal cells and systems2026
The double-edged sword of regulatory T cells in MASLD: from inflammation control to fibrosis promotion.
Review in Animal cells and systems, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- Cathepsin A deficiency exacerbates LPS-induced inflammatory liver injury and apoptosis.Animal cells and systems · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Metabolic dysfunction-associated steatotic liver disease (MASLD) and its advanced inflammatory subtype, metabolic dysfunction-associated steatohepatitis (MASH), are becoming increasingly prevalent liver disorders driven by complex interactions between metabolic stress, immune dysregulation, and fibrotic remodeling. Regulatory T cells (Tregs), traditionally recognized for their immunosuppressive functions, have emerged as key modulators of hepatic inflammation, fibrosis, and systemic metabolic balance. While Tregs can suppress pro-inflammatory immune responses and mitigate liver injury, accumulating evidence highlights their paradoxical roles in liver fibrosis, including the promotion of hepatic stellate cell activation and profibrotic remodeling. This review critically examines the dual and context-dependent roles of Tregs in MASLD and MASH, emphasizing implications for therapeutic intervention. Additionally, we discuss current preclinical strategies aimed at modulating Treg abundance and function, highlighting the challenges and opportunities associated with developing stage-specific therapeutic approaches that consider not only local hepatic effects but also potential systemic metabolic consequences.
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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 Socratic graph.