Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0015695 (fatty liver)
 13,941 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Parvovirus of Aleutian disease causes mainly damage to kidneys, but immune complexes deposition and damage may occur also in other organs. In mink farms of Latvia the liver dystrophy or hepatic lipidosis of mink is widely distributed. The goal of this study was to examine probability of liver damage and regeneration of mink infected with Aleutian disease virus. Liver injury was assessed histologically. The mink liver demonstrated inflammation of liver parenchyma and foci of fatty liver. In immunohistochemistry, during liver regeneration the matrix metalloproteinases MMP-9, vascular endothelial growth factor and beta-defensin 2 expressions were lower, but MMP-2 and nerve growth factor receptor p75 expression was increased.
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PMID:Histopathologic and immunohistochemical lesions in liver of mink infected with Aleutian disease virus. 2152 14

The phosphodiesterase family is involved in a wide spectrum of diseases, including ischemic stroke. However, few studies have analyzed the relationship between phosphodiesterase 4D (PDE4D) and myocardial infarction (MI). Therefore, the aim of this research was to evaluate the association of the PDE4D gene polymorphisms with MI, and with cardiometabolic parameters in the Mexican population. Six polymorphisms (rs2910829, rs1423246, rs966221, rs4502776, rs13172481, and rs6869495) were genotyped in 1023 MI patients and 1105 healthy controls. A similar distribution of the six polymorphisms was observed in both studied groups. However, after evaluating the linkage disequilibrium, we detected a risk haplotype for MI (AGAGAA; OR = 1.148; P = 0.025). In addition, the polymorphisms were associated with the presence of some clinical and metabolic parameters (central obesity, hypertriglyceridemia, Aspartate transaminase >p75, Lipoprotein (a) >30 mg/dL, TAT >p75, fatty liver, and vitamin D <30 ng/dL) in healthy controls. The results suggest that in the Mexican population, a PDE4D haplotype is associated with increased risk of developing MI, and that PDE4D polymorphisms are independently associated with the presence of cardiometabolic parameters.
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PMID:A haplotype of the phosphodiesterase 4D (PDE4D) gene is associated with myocardial infarction and with cardiometabolic parameters: the GEA study. 3071 79

Lipid-induced toxicity is part of several human diseases, but the mechanisms involved are not fully understood. Fatty liver is characterized by the expression of different growth and tissue factors. The neurotrophin, nerve growth factor (NGF) and its pro-form, pro-NGF, are present in fatty liver together with p75 neurotrophin receptor (p75NTR). Stimulation of human Huh7 hepatocyte cells with NGF and pro-NGF induced Sterol-regulator-element-binding protein-2 (SREBP2) activation and increased Low-Density Lipoprotein Receptor (LDLR) expression. We observed that phosphorylation of caspase-2 by p38 MAPK was essential for this regulation involving a caspase-3-mediated cleavage of SREBP2. RNA sequencing showed that several genes involved in lipid metabolism were altered in p75NTR-deficient mouse liver. The same lipogenic genes were downregulated in p75NTR gene-engineered human Huh7 cells and reciprocally upregulated by stimulation of p75NTRs. In the knock-out mice the serum cholesterol and triglyceride levels were reduced, suggesting a physiological role of p75NTRs in whole-body lipid metabolism. Taken together, this study shows that p75NTR signaling influences a network of genes involved in lipid metabolism in liver and hepatocyte cells. Modulation of p75NTR signaling may be a target to consider in various metabolic disorders accompanied by increased lipid accumulation.
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PMID:Caspase-2 and p75 neurotrophin receptor (p75NTR) are involved in the regulation of SREBP and lipid genes in hepatocyte cells. 3129 46

Neuregulin 4 (Nrg4) play important roles in the pathogenesis of obesity-associated disorders, including type 2 diabetes mellitus (T2DM) and nonalcoholic fatty liver disease (NAFLD). This study aims to investigate roles of Nrg4 in the pathophysiologic mechanism underlying the progression of tubulointerstitial fibrosis (TIF) in diabetic nephropathy (DN). In present study, Nrg4 is under-expression in serum and renal tissue of diabetic nephropathy rats. In present study, Nrg4 attenuate renal function injury, tubulointerstitial fibrosis, inflammation and suppress the expression levels of advanced glycosylation end products (AGEs) in vivo and vitro. Furthermore, the results reveal that Nrg4 ameliorates fibrosis and attenuate the expression of AGEs and inflammation via TNF-R1 signaling instead of TNF-R2 signaling in HK-2 cells. In conclusion, these results revealed that Nrg4 may effectively ameliorates TIF and attenuate the expression of AGEs in DN through TNF-R1 signaling instead of TNF-R2 signaling. We have provided evidence indicating that Nrg4 possesses therapeutic effect on TIF in DN.
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PMID:Neuregulin 4 attenuate tubulointerstitial fibrosis and advanced glycosylation end products accumulation in diabetic nephropathy rats via regulating TNF-R1 signaling. 3163 25