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Biomedicine & pharmacotherapy, 2023-09, Vol.165, p.115134-115134, Article 115134
2023
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Autor(en) / Beteiligte
Titel
Advances in the interaction between endoplasmic reticulum stress and osteoporosis
Ist Teil von
  • Biomedicine & pharmacotherapy, 2023-09, Vol.165, p.115134-115134, Article 115134
Ort / Verlag
France: Elsevier Masson SAS
Erscheinungsjahr
2023
Quelle
EZB Electronic Journals Library
Beschreibungen/Notizen
  • The endoplasmic reticulum (ER) is the main site for protein synthesis, folding, and secretion, and accumulation of the unfolded/misfolded proteins in the ER may induce ER stress. ER stress is an important participant in various intracellular signaling pathways. Prolonged- or high-intensity ER stress may induce cell apoptosis. Osteoporosis, characterized by imbalanced bone remodeling, is a global disease caused by many factors, such as ER stress. ER stress stimulates osteoblast apoptosis, increases bone loss, and promotes osteoporosis development. Many factors, such as the drug’s adverse effects, metabolic disorders, calcium ion imbalance, bad habits, and aging, have been reported to activate ER stress, resulting in the pathological development of osteoporosis. Increasing evidence shows that ER stress regulates osteogenic differentiation, osteoblast activity, and osteoclast formation and function. Various therapeutic agents have been developed to counteract ER stress and thereby suppress osteoporosis development. Thus, inhibition of ER stress has become a potential target for the therapeutic management of osteoporosis. However, the in-depth understanding of ER stress in the pathogenesis of osteoporosis still needs more effort. [Display omitted] •ER stress is implicated in bone remodeling.•ER stress mediates osteogenic differentiation and osteoblast activity.•ER stress regulates osteoclast formation and function.•ER stress has become a target for osteoporosis treatment.
Sprache
Englisch
Identifikatoren
ISSN: 0753-3322
eISSN: 1950-6007
DOI: 10.1016/j.biopha.2023.115134
Titel-ID: cdi_doaj_primary_oai_doaj_org_article_11945ccaba1a43f0a2f5f87596cc6555

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