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Statistic
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Details for phenotype: fibrosis
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EndoNet ID: ENP00473
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Name
fibrosis
General information
This phenotype is pathologic
Links to other resources
GO
regulation of tissue remodeling
MeSH term
D005355
Phenotype triggers
more activity (high ligand concentration, overexpression) of
Lysophosphatidic acid receptor 1
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in
kidney
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Fibrosis, the formation of excess fibrous connective tissues, is associated with a number of pathological conditions. Recently, a new aspect of LPA1 signaling has been uncovered in tubulointerstitial fibrosis (TIF), suggesting LPA1 signaling as a new therapeutic target in this disease.
[1]
Likewise, in a unilateral ureteral obstruction model for TIF, the resulting kidney fibrosis was accompanied by an increase in LPA accumulation and LPA1 expression.
[1]
Fibrosis was markedly reduced in Lpar1−/− mice or following treatment with Ki16425, an LPA1/LPA3 antagonist.
[1]
more activity (high ligand concentration, overexpression) of
mineralcorticoid receptor
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in
macrophage
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In renal disease models, reduced monocyte/macrophage infiltration is accompanied by a substantial reduction in fibrosis. MR signalling and macrophages appear to be important in inflammatory conditions in the kidney.
[2]
Activation of an MR, in the context of inappropriate sodium status, has major cardiovascular pathophysiological consequences including cardiac fibrosis.
[2]
In cardiac disease models, reduced monocyte/macrophage infiltration is accompanied by a substantial reduction in fibrosis. MR signalling and macrophages appear to be important in inflammatory conditions in the heart.
[2]
Selective deletion of MR from macrophages protected against mineralocorticoid-mediated cardiac fibrosis, despite normal macrophage recruitment.
[2]
Reference