ReviewArquivos de gastroenterologia2025
LIPOTOXICITY PLAYS A KEY ROLE IN THE DEVELOPMENT OF ANGIOGENESIS AND MICROCIRCULATORY MODULATION IN MASLD SPECTRUM.
Review in Arquivos de gastroenterologia, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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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
2 citing papers in PubMed.
- Hydroxysafflor yellow A attenuates microcirculatory disturbance in MAFLD via the EGFR/MAPK1 pathway.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundChronic liver diseases (CLDs), particularly metabolic-associated steatotic liver disease (MASLD), represent a significant global health burden, with potential progression to fibrosis, portal hypertension, and hepatocellular carcinoma (HCC). This review explores the role of vascular remodeling and angioarchitecture in MASLD pathogenesis, emphasizing the importance of microvascular changes, endothelial dysfunction, and angiogenesis in disease progression. Hepatic steatosis leads to hepatocyte enlargement and sinusoidal compression, disrupting microcirculation and oxygenation. Lipotoxicity, which is driven by excess fatty acids and oxidative stress, triggers inflammation and vascular permeability, fostering a proangiogenic environment. Capillarization of liver sinusoidal endothelial cells (LSECs) and activation of hepatic stellate cells (HSCs) contribute to fibrosis and neovascularization. Angiogenesis, especially via VEGF and other cytokines, is implicated in the transition from steatosis to steatohepatitis (MASH) and ultimately HCC, even in non-cirrhotic livers. Notably, portal hypertension may develop early in MASLD, independent of cirrhosis. Given the central role of vascular alterations in MASLD, future therapies may target endothelial and stromal cell interactions. Further research is needed to delineate disease-specific mechanisms and their implications for fibrosis and carcinogenesis.
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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 OpenQuestion graph.