Reversion inducing cysteine rich protein with Kazal motifs and cardiovascular diseases: The RECKlessness of adverse remodeling.
Adverse remodeling
EGFR
Fibrosis
Inflammation
Metallopeptidases
RECK
Journal
Cellular signalling
ISSN: 1873-3913
Titre abrégé: Cell Signal
Pays: England
ID NLM: 8904683
Informations de publication
Date de publication:
07 2021
07 2021
Historique:
received:
18
01
2021
revised:
23
03
2021
accepted:
24
03
2021
pubmed:
31
3
2021
medline:
20
1
2022
entrez:
30
3
2021
Statut:
ppublish
Résumé
The Reversion Inducing Cysteine Rich Protein With Kazal Motifs (RECK) is a glycosylphosphatidylinositol (GPI) anchored membrane-bound regulator of matrix metalloproteinases (MMPs). It is expressed throughout the body and plays a role in extracellular matrix (ECM) homeostasis and inflammation. In initial studies, RECK expression was found to be downregulated in various invasive cancers and associated with poor prognostic outcome. Restoring RECK, however, has been shown to reverse the metastatic phenotype. Downregulation of RECK expression is also reported in non-malignant diseases, such as periodontal disease, renal fibrosis, and myocardial fibrosis. As such, RECK induction has therapeutic potential in several chronic diseases. Mechanistically, RECK negatively regulates various matrixins involved in cell migration, proliferation, and adverse remodeling by targeting the expression and/or activation of multiple MMPs, A Disintegrin And Metalloproteinase Domain-Containing Proteins (ADAMs), and A Disintegrin And Metalloproteinase With Thrombospondin Motifs (ADAMTS). Outside of its role in remodeling, RECK has also been reported to exert anti-inflammatory effects. In cardiac diseases, for example, it has been shown to counteract several downstream effectors of Angiotensin II (Ang-II) that play a role in adverse cardiac and vascular remodeling, such as Interleukin-6 (IL-6)/IL-6 receptor (IL-6R)/glycoprotein 130 (IL-6 signal transducer) signaling and Epidermal Growth Factor Receptor (EGFR) transactivation. This review article focuses on the current understanding of the multifunctional effects of RECK and how its downregulation may contribute to adverse cardiovascular remodeling.
Identifiants
pubmed: 33781845
pii: S0898-6568(21)00081-4
doi: 10.1016/j.cellsig.2021.109993
pmc: PMC8204737
mid: NIHMS1688392
pii:
doi:
Substances chimiques
GPI-Linked Proteins
0
RECK protein, human
0
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, U.S. Gov't, Non-P.H.S.
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
109993Subventions
Organisme : BLRD VA
ID : I01 BX004220
Pays : United States
Organisme : BLRD VA
ID : IK6 BX004016
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL136386
Pays : United States
Informations de copyright
Published by Elsevier Inc.
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