International Journal of Molecular Sciences

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Dear Colleagues,

Osteoporosis is one of the most common metabolic bone diseases. Osteoporotic fractures, which represent a growing economic burden on global healthcare systems, impair quality of life and increase morbidity and mortality. In health, bone homeostasis encompasses coordinated dynamic equilibrium between bone-forming cells (osteoblasts) and bone-resorbing cells (osteoclasts). Mechanical stress is crucial for bone homeostasis and decreased mechanical loading is an established cause of bone loss and osteoporosis. Osteocytes, the most abundant and long-lived bone cells, are terminally differentiated osteoblasts that have a mechanosensory role and have emerged as a master regular of bone homeostasis. Osteocytes produce endocrine and paracrine factors, and this activity is regulated by mechanical stress as well as osteotropic factors such as, oestrogen, vitamin D and parathyroid hormone. This Special Issue explores intricate intra- and intercellular molecular signalling in bone cells in health and osteoporosis.

Dr. Harish K. Datta
Guest Editor

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Keywords

osteoporosis
bone
signalling
molecular
fractures
endocrine
paracrine

Published Papers (1 paper)

Research

15 pages, 1820 KiB

Open AccessArticle

Identification of Transcripts with Shared Roles in the Pathogenesis of Postmenopausal Osteoporosis and Cardiovascular Disease

by Sjur Reppe, Sveinung Gundersen, Geir K. Sandve, Yunpeng Wang, Ole A. Andreassen, Carolina Medina-Gomez, Fernando Rivadeneira, Tor P. Utheim, Eivind Hovig and Kaare M. Gautvik

Int. J. Mol. Sci. 2024, 25(10), 5554; https://doi.org/10.3390/ijms25105554 - 20 May 2024

Viewed by 547

Abstract

Epidemiological evidence suggests existing comorbidity between postmenopausal osteoporosis (OP) and cardiovascular disease (CVD), but identification of possible shared genes is lacking. The skeletal global transcriptomes were analyzed in trans-iliac bone biopsies (n = 84) from clinically well-characterized postmenopausal women (50 to 86 years) without clinical CVD using microchips and RNA sequencing. One thousand transcripts highly correlated with areal bone mineral density (aBMD) were further analyzed using bioinformatics, and common genes overlapping with CVD and associated biological mechanisms, pathways and functions were identified. Fifty genes (45 mRNAs, 5 miRNAs) were discovered with established roles in oxidative stress, inflammatory response, endothelial function, fibrosis, dyslipidemia and osteoblastogenesis/calcification. These pleiotropic genes with possible CVD comorbidity functions were also present in transcriptomes of microvascular endothelial cells and cardiomyocytes and were differentially expressed between healthy and osteoporotic women with fragility fractures. The results were supported by a genetic pleiotropy-informed conditional False Discovery Rate approach identifying any overlap in single nucleotide polymorphisms (SNPs) within several genes encoding aBMD- and CVD-associated transcripts. The study provides transcriptional and genomic evidence for genes of importance for both BMD regulation and CVD risk in a large collection of postmenopausal bone biopsies. Most of the transcripts identified in the CVD risk categories have no previously recognized roles in OP pathogenesis and provide novel avenues for exploring the mechanistic basis for the biological association between CVD and OP. Full article

(This article belongs to the Special Issue Molecular Biology of Osteoporosis)

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