ReviewClinics and research in hepatology and gastroenterology2015
Morphogen-related therapeutic targets for liver fibrosis.
Review in Clinics and research in hepatology and gastroenterology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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
4 citing papers in PubMed, 11 citations in OpenAlex.
- IOX1 protects from TGF-β induced fibrosis in LX-2 cells via the regulation of extracellular matrix protein expression.Experimental and therapeutic medicine · 2021Article
- Loss of pericyte smoothened activity in mice with genetic deficiency of leptin.BMC cell biology · 2017Article
- Article
- Hedgehog regulates yes-associated protein 1 in regenerating mouse liver.Hepatology (Baltimore, Md.) · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Recent research on hepatic stellate cells (HSCs) has spotlighted the involvement of morphogens in their cell fate determination in liver fibrosis. Temporally and spatially expressed during embryonic development, morphogens are involved in regulation of cell proliferation and differentiation, and tissue patterning. In normal adult liver, morphogens are generally expressed at low levels. However, in liver disease, myofibroblastic HSCs express morphogens such as Wnt, Shh, Necdin, DLK1, and Notch as part of their participation in fibrogenesis and wound healing. Liver regeneration involves cell proliferation and differentiation akin to embryonic liver development where the cells appear to undergo similar fates, and not surprisingly the morphogens are re-activated for the regenerative purpose in adult liver injury. Evidence also points to crosstalk of these morphogens in regulation of HSC fate determination. Genetic ablation or pharmacologic inhibition of morphogens reverts activated HSC to quiescent cells in culture and attenuates progression of hepatic fibrosis. However, positive regulation of liver regeneration by the morphogens needs to be spared. Therapeutically, manipulation of morphogen activities in a cell type and phase-specific manner should offer new modalities for chronic liver disease.
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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.