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STAT3-mediated osteogenesis and osteoclastogenesis in osteoporosis

Osteoporosis is a common skeletal disease with marked bone loss, deterioration of the bone microstructure and bone fragility. An abnormal bone remodelling cycle with relatively increased bone resorption is the crucial pathophysiological mechanism. Bone remodelling is predominantly controlled by oste...

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Autores principales: Hou, Xiaoli, Tian, Faming
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9310501/
https://www.ncbi.nlm.nih.gov/pubmed/35879773
http://dx.doi.org/10.1186/s12964-022-00924-1
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author Hou, Xiaoli
Tian, Faming
author_facet Hou, Xiaoli
Tian, Faming
author_sort Hou, Xiaoli
collection PubMed
description Osteoporosis is a common skeletal disease with marked bone loss, deterioration of the bone microstructure and bone fragility. An abnormal bone remodelling cycle with relatively increased bone resorption is the crucial pathophysiological mechanism. Bone remodelling is predominantly controlled by osteoblasts and osteoclasts, which are specialized cell types that are regulated by a variety of osteogenic and osteoclastic factors, including cytokines expressed within the bone microenvironment under local or systemic inflammatory conditions. Signal transducer and activator of transcription 3 (STAT3) plays a prominent role in the communication between cytokines and kinases by binding downstream gene promotors and is involved in a wide range of biological or pathological processes. Emerging evidence suggests that STAT3 and its network participate in bone remodelling and the development of osteoporosis, and this factor may be a potent target for osteoporosis treatment. This review focuses on the role and molecular mechanism of the STAT3 signalling pathway in osteogenesis, osteoclastogenesis and osteoporosis, particularly the bone-related cytokines that regulate the osteoblastic differentiation of bone marrow stromal cells and the osteoclastic differentiation of bone marrow macrophages by initiating STAT3 signalling. This review also examines the cellular interactions among immune cells, haematopoietic cells and osteoblastic/osteoclastic cells. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12964-022-00924-1.
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spelling pubmed-93105012022-07-26 STAT3-mediated osteogenesis and osteoclastogenesis in osteoporosis Hou, Xiaoli Tian, Faming Cell Commun Signal Review Osteoporosis is a common skeletal disease with marked bone loss, deterioration of the bone microstructure and bone fragility. An abnormal bone remodelling cycle with relatively increased bone resorption is the crucial pathophysiological mechanism. Bone remodelling is predominantly controlled by osteoblasts and osteoclasts, which are specialized cell types that are regulated by a variety of osteogenic and osteoclastic factors, including cytokines expressed within the bone microenvironment under local or systemic inflammatory conditions. Signal transducer and activator of transcription 3 (STAT3) plays a prominent role in the communication between cytokines and kinases by binding downstream gene promotors and is involved in a wide range of biological or pathological processes. Emerging evidence suggests that STAT3 and its network participate in bone remodelling and the development of osteoporosis, and this factor may be a potent target for osteoporosis treatment. This review focuses on the role and molecular mechanism of the STAT3 signalling pathway in osteogenesis, osteoclastogenesis and osteoporosis, particularly the bone-related cytokines that regulate the osteoblastic differentiation of bone marrow stromal cells and the osteoclastic differentiation of bone marrow macrophages by initiating STAT3 signalling. This review also examines the cellular interactions among immune cells, haematopoietic cells and osteoblastic/osteoclastic cells. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12964-022-00924-1. BioMed Central 2022-07-25 /pmc/articles/PMC9310501/ /pubmed/35879773 http://dx.doi.org/10.1186/s12964-022-00924-1 Text en © The Author(s) 2022 https://creativecommons.org/licenses/by/4.0/Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) . The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/ (https://creativecommons.org/publicdomain/zero/1.0/) ) applies to the data made available in this article, unless otherwise stated in a credit line to the data.
spellingShingle Review
Hou, Xiaoli
Tian, Faming
STAT3-mediated osteogenesis and osteoclastogenesis in osteoporosis
title STAT3-mediated osteogenesis and osteoclastogenesis in osteoporosis
title_full STAT3-mediated osteogenesis and osteoclastogenesis in osteoporosis
title_fullStr STAT3-mediated osteogenesis and osteoclastogenesis in osteoporosis
title_full_unstemmed STAT3-mediated osteogenesis and osteoclastogenesis in osteoporosis
title_short STAT3-mediated osteogenesis and osteoclastogenesis in osteoporosis
title_sort stat3-mediated osteogenesis and osteoclastogenesis in osteoporosis
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9310501/
https://www.ncbi.nlm.nih.gov/pubmed/35879773
http://dx.doi.org/10.1186/s12964-022-00924-1
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