ArticleDigestive diseases and sciences2014
The role of phospholipase D1 in liver fibrosis induced by dimethylnitrosamine in vivo.
Article in Digestive diseases and sciences, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 8 citations in OpenAlex.
- Inhibition of phospholipase D1 ameliorates hepatocyte steatosis and non-alcoholic fatty liver disease.JHEP reports : innovation in hepatology · 2023Article
- Role of phospholipase D in bleomycin-induced mitochondrial reactive oxygen species generation, mitochondrial DNA damage, and pulmonary fibrosis.American journal of physiology. Lung cellular and molecular physiology · 2019Article
- Phospholipase D1 deficiency in mice causes nonalcoholic fatty liver disease via an autophagy defect.Scientific reports · 2016Article
- Physiological and pathophysiological roles for phospholipase D.Journal of lipid research · 2015Review
- Gene expression profiling of extrahepatic ducts in children with biliary atresia.International journal of clinical and experimental medicine · 2015Article
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundPhospholipase D (PLD) has been proved to be involved in regulating function of fibroblasts and might play a role in mediating organic fibrosis.
aimsTo investigate the role and mechanism of PLD on dimethylnitrosamine (DMN)-induced rat liver fibrosis.
methodsFifty-five male Wistar rats were divided into normal control group, DMN model group, N-methylethanolamine (MEA) control group, and MEA-intervention group. We observed the effects of MEA, a PLD inhibitor on the development and progression of rat liver fibrosis by comparing the physical and biochemical indexes, tissue pathology, PLD activity, and typical markers and cytokines related to fibrosis in the four groups.
resultsAccompanied by the down-regulation of PLD1 expression, the MEA-intervention group had improved outcomes compared with the DMN model group in terms of spleen weight, spleen/weight index, serum and tissue biochemical indexes, tissue hydroxyproline, and tissue pathology. The MEA-intervention group had lower TIMP1, COL1A1, and higher MMPs expression level than the DMN model group. The activity of PLD and PLD1, α-SMA expression level in the MEA-intervention group was much lower than those in the DMN model group. There was no significant difference between the two groups in the expression level of TGF-β1 and MCP1. Meanwhile, there were no significant differences between normal control group and MEA control group in the parameters stated above.
conclusionPhospholipase D1 may play an important role in the development and progression of rat liver fibrosis. Inhibition of PLD may become a new strategy to prevent or alleviate liver fibrosis.
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