ArticleHepatology communications2025
Induction of TFEB promotes Kupffer cell survival and reduces lipid accumulation in MASLD.
Article in Hepatology communications, 2025. 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.
- Short histological kaleidoscope - recent findings in histology. Part VI. Kupffer cells, hepatic stellate cells, enteroendocrine cells, and telocytes.Romanian journal of morphology and embryology = Revue roumaine de morphologie et embryologieReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
19 authors.
Funding
Abstract
backgroundKupffer cells (KCs) are the tissue-resident macrophages of the liver, where they serve a critical role in maintaining liver tissue homeostasis and act as a filter for circulation. The composition of hepatic macrophages changes during metabolic dysfunction-associated liver disease (MASLD), with the loss of resident KCs being a hallmark of disease progression. The mechanism(s) and consequences of KC death in metabolic liver disease have yet to be defined. Transcription factor EB (TFEB) is a master regulator of lysosome function and lipid metabolism, which has been shown to protect macrophages from lipid stress in atherosclerosis. We hypothesized that TFEB would improve KC fitness in MASLD.
methodsTo investigate the potential beneficial effect of TFEB induction in KCs, we created a transgenic mouse in which TFEB was overexpressed specifically in KCs and evaluated its impact on disease pathogenesis in high-fat, high-sucrose (HFHS) and choline-deficient diet models of MASLD.
resultsWe found that TFEB induction protected KCs from cell death in both models of MASLD. KC preservation through TFEB induction reduced liver steatosis with HFHS diet via mechanisms that were dependent on macrophage lysosomal lipolysis and mitochondrial fatty acid oxidation. Fibrosis was unchanged in choline-deficient diet studies. TFEB protected KCs from cell death by diminishing oxidative stress and reducing ferroptosis through a mechanism that involved enhanced NADPH levels.
conclusionsTFEB induction promotes KC fitness upon lipid stress during MASLD. Preservation of lipid-adapted KCs demonstrates beneficial effects against liver steatosis and protects portal filtration during MASLD.
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.