Cargando…

RCAN1 in cardiovascular diseases: molecular mechanisms and a potential therapeutic target

Cardiovascular diseases (CVDs) are the leading cause of mortality worldwide. Considerable efforts are needed to elucidate the underlying mechanisms for the prevention and treatment of CVDs. Regulator of calcineurin 1 (RCAN1) is involved in both development/maintenance of the cardiovascular system an...

Descripción completa

Detalles Bibliográficos
Autores principales: Wang, Shuai, Wang, Yuqing, Qiu, Kaixin, Zhu, Jin, Wu, Yili
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7709393/
https://www.ncbi.nlm.nih.gov/pubmed/33267791
http://dx.doi.org/10.1186/s10020-020-00249-0
_version_ 1783617740701958144
author Wang, Shuai
Wang, Yuqing
Qiu, Kaixin
Zhu, Jin
Wu, Yili
author_facet Wang, Shuai
Wang, Yuqing
Qiu, Kaixin
Zhu, Jin
Wu, Yili
author_sort Wang, Shuai
collection PubMed
description Cardiovascular diseases (CVDs) are the leading cause of mortality worldwide. Considerable efforts are needed to elucidate the underlying mechanisms for the prevention and treatment of CVDs. Regulator of calcineurin 1 (RCAN1) is involved in both development/maintenance of the cardiovascular system and the pathogenesis of CVDs. RCAN1 reduction protects against atherosclerosis by reducing the uptake of oxidized low-density lipoproteins, whereas RCAN1 has a protective effect on myocardial ischemia/reperfusion injury, myocardial hypertrophy and intramural hematoma/aortic rupture mainly mediated by maintaining mitochondrial function and inhibiting calcineurin and Rho kinase activity, respectively. In this review, the regulation and the function of RCAN1 are summarized. Moreover, the dysregulation of RCAN1 in CVDs is reviewed. In addition, the beneficial role of RCAN1 reduction in atherosclerosis and the protective role of RCAN1 in myocardial ischemia/reperfusion injury, myocardial hypertrophy and intramural hematoma /aortic rupture are discussed, as well as underlying mechanisms. Furthermore, the therapeutic potential and challenges of targeting RCAN1 for CVDs treatment are also discussed.
format Online
Article
Text
id pubmed-7709393
institution National Center for Biotechnology Information
language English
publishDate 2020
publisher BioMed Central
record_format MEDLINE/PubMed
spelling pubmed-77093932020-12-03 RCAN1 in cardiovascular diseases: molecular mechanisms and a potential therapeutic target Wang, Shuai Wang, Yuqing Qiu, Kaixin Zhu, Jin Wu, Yili Mol Med Mini-Review Cardiovascular diseases (CVDs) are the leading cause of mortality worldwide. Considerable efforts are needed to elucidate the underlying mechanisms for the prevention and treatment of CVDs. Regulator of calcineurin 1 (RCAN1) is involved in both development/maintenance of the cardiovascular system and the pathogenesis of CVDs. RCAN1 reduction protects against atherosclerosis by reducing the uptake of oxidized low-density lipoproteins, whereas RCAN1 has a protective effect on myocardial ischemia/reperfusion injury, myocardial hypertrophy and intramural hematoma/aortic rupture mainly mediated by maintaining mitochondrial function and inhibiting calcineurin and Rho kinase activity, respectively. In this review, the regulation and the function of RCAN1 are summarized. Moreover, the dysregulation of RCAN1 in CVDs is reviewed. In addition, the beneficial role of RCAN1 reduction in atherosclerosis and the protective role of RCAN1 in myocardial ischemia/reperfusion injury, myocardial hypertrophy and intramural hematoma /aortic rupture are discussed, as well as underlying mechanisms. Furthermore, the therapeutic potential and challenges of targeting RCAN1 for CVDs treatment are also discussed. BioMed Central 2020-12-02 /pmc/articles/PMC7709393/ /pubmed/33267791 http://dx.doi.org/10.1186/s10020-020-00249-0 Text en © The Author(s) 2020 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/.
spellingShingle Mini-Review
Wang, Shuai
Wang, Yuqing
Qiu, Kaixin
Zhu, Jin
Wu, Yili
RCAN1 in cardiovascular diseases: molecular mechanisms and a potential therapeutic target
title RCAN1 in cardiovascular diseases: molecular mechanisms and a potential therapeutic target
title_full RCAN1 in cardiovascular diseases: molecular mechanisms and a potential therapeutic target
title_fullStr RCAN1 in cardiovascular diseases: molecular mechanisms and a potential therapeutic target
title_full_unstemmed RCAN1 in cardiovascular diseases: molecular mechanisms and a potential therapeutic target
title_short RCAN1 in cardiovascular diseases: molecular mechanisms and a potential therapeutic target
title_sort rcan1 in cardiovascular diseases: molecular mechanisms and a potential therapeutic target
topic Mini-Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7709393/
https://www.ncbi.nlm.nih.gov/pubmed/33267791
http://dx.doi.org/10.1186/s10020-020-00249-0
work_keys_str_mv AT wangshuai rcan1incardiovasculardiseasesmolecularmechanismsandapotentialtherapeutictarget
AT wangyuqing rcan1incardiovasculardiseasesmolecularmechanismsandapotentialtherapeutictarget
AT qiukaixin rcan1incardiovasculardiseasesmolecularmechanismsandapotentialtherapeutictarget
AT zhujin rcan1incardiovasculardiseasesmolecularmechanismsandapotentialtherapeutictarget
AT wuyili rcan1incardiovasculardiseasesmolecularmechanismsandapotentialtherapeutictarget