6533b853fe1ef96bd12ac14f
RESEARCH PRODUCT
Fibrosis markers and CRIM1 increase in chronic heart failure of increasing severity.
Franco Tarro GentaFabio Luigi Massimo RicciardoloDavide VallesePantaleo GiannuzziErmanno EleuteriLorena Delle DonneFrancesco CappelloAlessandro PitruzzellaIsabella GnemmiAntonino Di Stefanosubject
medicine.medical_specialtyHealth Toxicology and MutagenesisClinical BiochemistryInflammationBiochemistryGastroenterologySeverity of Illness IndexBone morphogenetic protein 1ElectrocardiographyFibrosisInternal medicinemedicineEndothelial dysfunction heart fibrosis inflammationHumanscardiovascular diseasesEndothelial dysfunctionHeart Failurebusiness.industryMembrane ProteinsBone Morphogenetic Protein Receptorsmedicine.diseaseFibulinProcollagen peptidaseHeart failureImmunologyChronic Diseasecardiovascular systemBAMBImedicine.symptombusinesscirculatory and respiratory physiologydescription
AbstractBackground: Fibrosis suppressors/activators in chronic heart failure (CHF) is a topic of investigation.Aim: To quantify serum levels of fibrosis regulators in CHF.Methods: ELISA tests were used to quantify fibrosis regulators, procollagen type-(PIP)I, (PIP)III, collagen-I, III, BMP1,2,3,7, SDF1α, CXCR4, fibulin 1,2,3, BMPER, CRIM1 and BAMBI in 66 CHF (NYHA class I, n = 9; II, n = 34; III n = 23), and in 14 controls.Results: In CHF, TGFβR2, PIPIII, SDF1α and CRIM1 were increased. PIPIII correlated with CRIM1.Conclusions: The BMPs inhibitor CRIM1 is increased and correlates with higher levels of serum PIPIII showing an imbalance in favor of pro-fibrotic mechanisms in CHF.
| year | journal | country | edition | language |
|---|---|---|---|---|
| 2014-03-11 |