ATP-induced cell death: a novel hypothesis for osteoporosis

ATP-induced cell death has emerged as a captivating realm of inquiry with profound ramifications in the context of osteoporosis. This study unveils a paradigm-shifting hypothesis that illuminates the prospective involvement of ATP-induced cellular demise in the etiology of osteoporosis. Initially, w...

Full description

Saved in:
Bibliographic Details
Published inFrontiers in cell and developmental biology Vol. 11; p. 1324213
Main Authors Wang, Wei, Zhang, Haolong, Sandai, Doblin, Zhao, Rui, Bai, Jinxia, Wang, Yanfei, Wang, Yong, Zhang, Zhongwen, Zhang, Hao-Ling, Song, Zhi-Jing
Format Journal Article
LanguageEnglish
Published Switzerland Frontiers Media S.A 2023
Subjects
Online AccessGet full text

Cover

Loading…
More Information
Summary:ATP-induced cell death has emerged as a captivating realm of inquiry with profound ramifications in the context of osteoporosis. This study unveils a paradigm-shifting hypothesis that illuminates the prospective involvement of ATP-induced cellular demise in the etiology of osteoporosis. Initially, we explicate the morphological attributes of ATP-induced cell death and delve into the intricacies of the molecular machinery and regulatory networks governing ATP homeostasis and ATP-induced cell death. Subsequently, our focus pivots towards the multifaceted interplay between ATP-induced cellular demise and pivotal cellular protagonists, such as bone marrow-derived mesenchymal stem cells, osteoblasts, and osteoclasts, accentuating their potential contributions to secondary osteoporosis phenotypes, encompassing diabetic osteoporosis, glucocorticoid-induced osteoporosis, and postmenopausal osteoporosis. Furthermore, we probe the captivating interplay between ATP-induced cellular demise and alternative modalities of cellular demise, encompassing apoptosis, autophagy, and necroptosis. Through an all-encompassing inquiry into the intricate nexus connecting ATP-induced cellular demise and osteoporosis, our primary goal is to deepen our comprehension of the underlying mechanisms propelling this malady and establish a theoretical bedrock to underpin the development of pioneering therapeutic strategies.
Bibliography:ObjectType-Article-2
SourceType-Scholarly Journals-1
ObjectType-Feature-3
content type line 23
ObjectType-Review-1
ISSN:2296-634X
2296-634X
DOI:10.3389/fcell.2023.1324213