Principles of the activin receptor signaling pathway and its inhibition.
Bone
Growth factor
Hematopoiesis
IASP
Muscle
Journal
Cytokine & growth factor reviews
ISSN: 1879-0305
Titre abrégé: Cytokine Growth Factor Rev
Pays: England
ID NLM: 9612306
Informations de publication
Date de publication:
08 2021
08 2021
Historique:
received:
29
03
2021
revised:
14
04
2021
accepted:
15
04
2021
pubmed:
3
5
2021
medline:
2
10
2021
entrez:
2
5
2021
Statut:
ppublish
Résumé
This review captures the anabolic and stimulatory effects observed with inhibition of the transforming growth factor β superfamily in muscle, blood, and bone. New medicinal substances that rectify activin, myostatin, and growth differentiation factor 11 signaling give hope to the many whose lives are affected by deterioration of these tissues. The review first covers the origin, structure, and common pathway of activins, myostatin, and growth differentiation factor 11 along with the pharmacodynamics of the new class of molecules designed to oppose the activin receptor signaling pathway. Current terminology surrounding this new class of molecules is inconsistent and does not infer functionality. Adopting inhibitors of the activin receptor signaling pathway (IASPs) as a generic term is proposed because it encapsulates the molecular mechanisms along the pathway trajectory. To conclude, a pragmatic classification of IASPs is presented that integrates functionality and side effects based on the data available from animals and humans. This provides researchers and clinicians with a tool to tailor IASPs therapy according to the need of projects or patients and with respect to side effects.
Identifiants
pubmed: 33933900
pii: S1359-6101(21)00034-4
doi: 10.1016/j.cytogfr.2021.04.001
pii:
doi:
Substances chimiques
Transforming Growth Factor beta
0
Activins
104625-48-1
Activin Receptors
EC 2.7.11.30
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
1-17Informations de copyright
Copyright © 2021 The Author(s). Published by Elsevier Ltd.. All rights reserved.