Plasminogen activator inhibitor-1 reduces cardiac fibrosis and promotes M2 macrophage polarization in inflammatory cardiomyopathy.
Adult
Aged
Cardiomyopathy, Dilated
/ immunology
Cell Differentiation
Female
Fibrosis
Humans
Macrophages
/ immunology
Male
Middle Aged
Myocardium
/ immunology
Myofibroblasts
/ immunology
Phenotype
Plasminogen Activator Inhibitor 1
/ metabolism
Retrospective Studies
Signal Transduction
Transforming Growth Factor beta1
/ genetics
Up-Regulation
Alpha-smooth muscle actin
Cardiac fibrosis
DCM
DCMi
Inflammatory cardiomyopathy
Macrophages
Monocytes
Myocarditis
Myofibroblast
PAI-1
TGF-β
Journal
Basic research in cardiology
ISSN: 1435-1803
Titre abrégé: Basic Res Cardiol
Pays: Germany
ID NLM: 0360342
Informations de publication
Date de publication:
11 01 2021
11 01 2021
Historique:
received:
15
10
2020
accepted:
15
12
2020
entrez:
12
1
2021
pubmed:
13
1
2021
medline:
15
12
2021
Statut:
epublish
Résumé
Plasminogen activator inhibitor-1 (PAI-1) has a cardioprotective function in mice by repressing cardiac fibrosis through TGF-β and plasminogen-mediated pathways. In addition it is known to be involved in the recruitment and polarization of monocytes/macrophages towards a M2 phenotype in cancer. Here, we investigated the expression of PAI-1 in human dilated cardiomyopathy (DCM) and inflammatory dilated cardiomyopathy (DCMi) and its effect on cardiac fibrosis and macrophage polarization. We retrospectively analyzed endomyocardial biopsies (EMBs) of patients with DCM or DCMi for PAI-1 expression by immunohistochemistry. Furthermore, EMBs were evaluated for the content of fibrotic tissue, number of activated myofibroblasts, TGF-β expression, as well as for M1 and M2 macrophages. Patients with high-grade DCMi (DCMi-high, CD3
Identifiants
pubmed: 33432417
doi: 10.1007/s00395-020-00840-w
pii: 10.1007/s00395-020-00840-w
pmc: PMC7801308
doi:
Substances chimiques
Plasminogen Activator Inhibitor 1
0
SERPINE1 protein, human
0
TGFB1 protein, human
0
Transforming Growth Factor beta1
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
1Subventions
Organisme : Deutsche Forschungsgemeinschaft
ID : CRC Transregio 19
Organisme : European Research Area Network on Cardiovascular Diseases (ERA-CVD)
ID : JTC2016-40-158
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