Details for phenotype: production of molecular mediator involved in inflammatory

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EndoNet ID: ENP00471

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Name

production of molecular mediator involved in inflammatory

General information

This phenotype is not pathologic

Links to other resources

GO	production of molecular mediator involved in inflammatory response
MeSH term	68007249

Phenotype triggers

• more activity (high ligand concentration, overexpression) of mineralcorticoid receptor ui-button
  in macrophage ui-button
  • Inflammation may be a key mechanism translating MR signalling into cardiac and vascular remodelling. [1]
  • Mineralocorticoid/salt-induced pathology is characterised by an early vascular inflammatory response with elevated cardiac expression of inflammatory mediators such as monocytes/macrophages, MCP-1 and adhesion molecules (ICAM-1 and VCAM-1), prior to the onset of collagen deposition. [2]
  • mineralocorticoid/salt treatment is also associated with increased monocyte/macrophage infiltration and expression of inflammatory markers such as osteopontin, MCP-1, IL-6 and IL-1β in the kidney. [3]
  • MR antagonism prevents inflammation-induced peritoneal fibrosis and reduces macrophage infiltration and expression of MCP-1, TGF-β, PAI-1 and Sgk-1. [4]

EndoNet at the Institut for Bioinformatics UMG Göttingen