Thrombospondin-1 in maladaptive aging responses: a concept whose time has come.
CD47
aging
cardiovascular and metabolic disease
self-renewal
senescence
thrombospondin-1
Journal
American journal of physiology. Cell physiology
ISSN: 1522-1563
Titre abrégé: Am J Physiol Cell Physiol
Pays: United States
ID NLM: 100901225
Informations de publication
Date de publication:
01 07 2020
01 07 2020
Historique:
pubmed:
7
5
2020
medline:
22
10
2020
entrez:
7
5
2020
Statut:
ppublish
Résumé
Numerous age-dependent alterations at the molecular, cellular, tissue and organ systems levels underlie the pathophysiology of aging. Herein, the focus is upon the secreted protein thrombospondin-1 (TSP1) as a promoter of aging and age-related diseases. TSP1 has several physiological functions in youth, including promoting neural synapse formation, mediating responses to ischemic and genotoxic stress, minimizing hemorrhage, limiting angiogenesis, and supporting wound healing. These acute functions of TSP1 generally require only transient expression of the protein. However, accumulating basic and clinical data reinforce the view that chronic diseases of aging are associated with accumulation of TSP1 in the extracellular matrix, which is a significant maladaptive contributor to the aging process. Identification of the relevant cell types that chronically produce and respond to TSP1 and the molecular mechanisms that mediate the resulting maladaptive responses could direct the development of therapeutic agents to delay or revert age-associated maladies.
Identifiants
pubmed: 32374675
doi: 10.1152/ajpcell.00089.2020
pmc: PMC7468894
doi:
Substances chimiques
Thrombospondin 1
0
Types de publication
Journal Article
Research Support, N.I.H., Intramural
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
C45-C63Subventions
Organisme : Intramural NIH HHS
ID : ZIA SC009172
Pays : United States
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