Skeletal-Vascular Interactions in Bone Development, Homeostasis, and Pathological Destruction

Bone is a highly vascularized organ that not only plays multiple roles in supporting the body and organs but also endows the microstructure, enabling distinct cell lineages to reciprocally interact. Recent studies have uncovered relevant roles of the bone vasculature in bone patterning, morphogenesi...

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Autores principales: Watanabe, Haruhisa, Maishi, Nako, Hoshi-Numahata, Marie, Nishiura, Mai, Nakanishi-Kimura, Atsuko, Hida, Kyoko, Iimura, Tadahiro
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2023
Materias:
Review
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10341726/
https://www.ncbi.nlm.nih.gov/pubmed/37446097
http://dx.doi.org/10.3390/ijms241310912
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author Watanabe, Haruhisa
Maishi, Nako
Hoshi-Numahata, Marie
Nishiura, Mai
Nakanishi-Kimura, Atsuko
Hida, Kyoko
Iimura, Tadahiro
author_facet Watanabe, Haruhisa
Maishi, Nako
Hoshi-Numahata, Marie
Nishiura, Mai
Nakanishi-Kimura, Atsuko
Hida, Kyoko
Iimura, Tadahiro
author_sort Watanabe, Haruhisa
collection PubMed
description Bone is a highly vascularized organ that not only plays multiple roles in supporting the body and organs but also endows the microstructure, enabling distinct cell lineages to reciprocally interact. Recent studies have uncovered relevant roles of the bone vasculature in bone patterning, morphogenesis, homeostasis, and pathological bone destruction, including osteoporosis and tumor metastasis. This review provides an overview of current topics in the interactive molecular events between endothelial cells and bone cells during bone ontogeny and discusses the future direction of this research area to find novel ways to treat bone diseases.
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spelling pubmed-103417262023-07-14 Skeletal-Vascular Interactions in Bone Development, Homeostasis, and Pathological Destruction Watanabe, Haruhisa Maishi, Nako Hoshi-Numahata, Marie Nishiura, Mai Nakanishi-Kimura, Atsuko Hida, Kyoko Iimura, Tadahiro Int J Mol Sci Review Bone is a highly vascularized organ that not only plays multiple roles in supporting the body and organs but also endows the microstructure, enabling distinct cell lineages to reciprocally interact. Recent studies have uncovered relevant roles of the bone vasculature in bone patterning, morphogenesis, homeostasis, and pathological bone destruction, including osteoporosis and tumor metastasis. This review provides an overview of current topics in the interactive molecular events between endothelial cells and bone cells during bone ontogeny and discusses the future direction of this research area to find novel ways to treat bone diseases. MDPI 2023-06-30 /pmc/articles/PMC10341726/ /pubmed/37446097 http://dx.doi.org/10.3390/ijms241310912 Text en © 2023 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).
spellingShingle Review
Watanabe, Haruhisa
Maishi, Nako
Hoshi-Numahata, Marie
Nishiura, Mai
Nakanishi-Kimura, Atsuko
Hida, Kyoko
Iimura, Tadahiro
Skeletal-Vascular Interactions in Bone Development, Homeostasis, and Pathological Destruction
title Skeletal-Vascular Interactions in Bone Development, Homeostasis, and Pathological Destruction
title_full Skeletal-Vascular Interactions in Bone Development, Homeostasis, and Pathological Destruction
title_fullStr Skeletal-Vascular Interactions in Bone Development, Homeostasis, and Pathological Destruction
title_full_unstemmed Skeletal-Vascular Interactions in Bone Development, Homeostasis, and Pathological Destruction
title_short Skeletal-Vascular Interactions in Bone Development, Homeostasis, and Pathological Destruction
title_sort skeletal-vascular interactions in bone development, homeostasis, and pathological destruction
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10341726/
https://www.ncbi.nlm.nih.gov/pubmed/37446097
http://dx.doi.org/10.3390/ijms241310912
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