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Minoxidil decreases collagen I deposition and tissue-like contraction in clubfoot-derived cells: a way to improve conservative treatment of relapsed clubfoot?
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SYSNO ASEP 0547576 Document Type J - Journal Article R&D Document Type Journal Article Subsidiary J Článek ve WOS Title Minoxidil decreases collagen I deposition and tissue-like contraction in clubfoot-derived cells: a way to improve conservative treatment of relapsed clubfoot? Author(s) Knitlová, Jarmila (FGU-C) RID, ORCID
Doubková, Martina (FGU-C) ORCID, RID
Plencner, Martin (FGU-C) RID, ORCID
Vondrášek, David (FGU-C) ORCID, SAI, RID
Eckhardt, Adam (FGU-C) RID, ORCID
Ošťádal, M. (CZ)
Musílková, Jana (FGU-C) RID, ORCID
Bačáková, Lucie (FGU-C) RID, ORCID
Novotný, T. (CZ)Source Title Connective Tissue Research. - : Taylor & Francis - ISSN 0300-8207
Roč. 62, č. 5 (2021), s. 554-569Number of pages 16 s. Language eng - English Country US - United States Keywords relapsed clubfoot ; congenital idiopathic talipes equinovarus ; CTEV ; fibrosis ; minoxidil ; collagen type I Subject RIV FI - Traumatology, Orthopedics OECD category Orthopaedics R&D Projects NV17-31564A GA MZd - Ministry of Health (MZ) LM2015062 GA MŠMT - Ministry of Education, Youth and Sports (MEYS) Method of publishing Open access Institutional support FGU-C - RVO:67985823 UT WOS 000571321300001 EID SCOPUS 85091144762 DOI https://doi.org/10.1080/03008207.2020.1816992 Annotation Clubfoot is a congenital deformity affecting the musculoskeletal system, resulting in contracted and stiff tissue in the medial part of the foot. Minoxidil (MXD) has an inhibitory effect on lysyl hydroxylase, which influences the quality of extracellular matrix crosslinking, and could therefore be used to reduce the stiffness and to improve the flexibility of the tissue. We assessed the in vitro antifibrotic effects of minoxidil on clubfoot-derived cells. Workplace Institute of Physiology Contact Lucie Trajhanová, lucie.trajhanova@fgu.cas.cz, Tel.: 241 062 400 Year of Publishing 2022 Electronic address https://doi.org/10.1080/03008207.2020.1816992
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