Annexin A2 in Fibrinolysis, Inflammation and Fibrosis.
angiogenesis
annexin A2
autoimmune disease
fibrinolysis
fibrosis
inflammation
thrombosis
tissue repair
Journal
International journal of molecular sciences
ISSN: 1422-0067
Titre abrégé: Int J Mol Sci
Pays: Switzerland
ID NLM: 101092791
Informations de publication
Date de publication:
25 Jun 2021
25 Jun 2021
Historique:
received:
20
05
2021
revised:
12
06
2021
accepted:
17
06
2021
entrez:
2
7
2021
pubmed:
3
7
2021
medline:
27
7
2021
Statut:
epublish
Résumé
As a cell surface tissue plasminogen activator (tPA)-plasminogen receptor, the annexin A2 (A2) complex facilitates plasmin generation on the endothelial cell surface, and is an established regulator of hemostasis. Whereas A2 is overexpressed in hemorrhagic disease such as acute promyelocytic leukemia, its underexpression or impairment may result in thrombosis, as in antiphospholipid syndrome, venous thromboembolism, or atherosclerosis. Within immune response cells, A2 orchestrates membrane repair, vesicle fusion, and cytoskeletal organization, thus playing a critical role in inflammatory response and tissue injury. Dysregulation of A2 is evident in multiple human disorders, and may contribute to the pathogenesis of various inflammatory disorders. The fibrinolytic system, moreover, is central to wound healing through its ability to remodel the provisional matrix and promote angiogenesis. A2 dysfunction may also promote tissue fibrogenesis and end-organ fibrosis.
Identifiants
pubmed: 34202091
pii: ijms22136836
doi: 10.3390/ijms22136836
pmc: PMC8268605
pii:
doi:
Substances chimiques
Annexin A2
0
Biomarkers
0
Types de publication
Journal Article
Review
Langues
eng
Sous-ensembles de citation
IM
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