Uterine Collagen Cross-Linking: Biology, Role in Disorders, and Therapeutic Implications.

Cervical ripening Collagen Cross-link LOX Uterine fibroids Uterus

Journal

Reproductive sciences (Thousand Oaks, Calif.)
ISSN: 1933-7205
Titre abrégé: Reprod Sci
Pays: United States
ID NLM: 101291249

Informations de publication

Date de publication:
31 Oct 2023
Historique:
received: 22 06 2023
accepted: 13 10 2023
medline: 1 11 2023
pubmed: 1 11 2023
entrez: 1 11 2023
Statut: aheadofprint

Résumé

Collagen is an essential constituent of the uterine extracellular matrix that provides biomechanical strength, resilience, structural integrity, and the tensile properties necessary for the normal functioning of the uterus. Cross-linking is a fundamental step in collagen biosynthesis and is critical for its normal biophysical properties. This step occurs enzymatically via lysyl oxidase (LOX) or non-enzymatically with the production of advanced glycation end-products (AGEs). Cross-links found in uterine tissue include the reducible dehydro-dihydroxylysinonorleucine (deH-DHLNL), dehydro-hydroxylysinonorleucine (deH-HLNL), and histidinohydroxymerodesmosine (HHMD); and the non-reducible pyridinoline (PYD), deoxy-pyridinoline (DPD); and a trace of pentosidine (PEN). Collagen cross-links are instrumental for uterine tissue integrity and the continuation of a healthy pregnancy. Decreased cervical cross-link density is observed in preterm birth, whereas increased tissue stiffness caused by increased cross-link density is a pathogenic feature of uterine fibroids. AGEs disrupt embryo development, decidualization, implantation, and trophoblast invasion. Uterine collagen cross-linking regulators include steroid hormones, such as progesterone and estrogen, prostaglandins, proteoglycans, metalloproteinases, lysyl oxidases, nitric oxide, nicotine, and vitamin D. Thus, uterine collagen cross-linking presents an opportunity to design therapeutic targets and warrants further investigation in common uterine disorders, such as uterine fibroids, cervical insufficiency, preterm birth, dystocia, endometriosis, and adenomyosis.

Identifiants

pubmed: 37907804
doi: 10.1007/s43032-023-01386-7
pii: 10.1007/s43032-023-01386-7
doi:

Types de publication

Journal Article Review

Langues

eng

Sous-ensembles de citation

IM

Subventions

Organisme : National Institute of Child Health and Human Development
ID : R01HD094380

Informations de copyright

© 2023. The Author(s), under exclusive licence to Society for Reproductive Investigation.

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Auteurs

Irem Kurt (I)

Department of Gynecology and Obstetrics, Johns Hopkins University School of Medicine, Baltimore, MD, 21205, USA.
Selcuk University Faculty of Medicine, 42000, Konya, Turkey.

Mehmet Kulhan (M)

Department of Gynecology and Obstetrics, Selcuk University Faculty of Medicine, 42000, Konya, Turkey.

Abdelrahman AlAshqar (A)

Department of Obstetrics, Gynecology and Reproductive Sciences, Yale School of Medicine, New Haven, CT, 06510, USA.

Mostafa A Borahay (MA)

Department of Gynecology and Obstetrics, Johns Hopkins University School of Medicine, Baltimore, MD, 21205, USA. mboraha1@jhmi.edu.

Classifications MeSH