Status
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Details for phenotype: fibrosis

EndoNet ID: ENP00473

Name

fibrosis

General information

This phenotype is pathologic

Links to other resources

GO
MeSH term D005355

Phenotype triggers

  • more activity (high ligand concentration, overexpression) of Lysophosphatidic acid receptor 1
    in kidney
    • 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
    in macrophage
    • 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