2022
Follistatin-like 1 and its paralogs in heart development and cardiovascular disease
HOŘÁK, Martin, DeLisa FAIRWEATHER, Piia Pauliina KOKKONEN, David BEDNÁŘ, Julie DOBROVOLNÁ et. al.Základní údaje
Originální název
Follistatin-like 1 and its paralogs in heart development and cardiovascular disease
Autoři
HOŘÁK, Martin (203 Česká republika, domácí), DeLisa FAIRWEATHER, Piia Pauliina KOKKONEN (246 Finsko, domácí), David BEDNÁŘ (203 Česká republika, domácí) a Julie DOBROVOLNÁ (203 Česká republika, garant, domácí)
Vydání
Heart Failure Reviews, New York, Springer US, 2022, 1382-4147
Další údaje
Jazyk
angličtina
Typ výsledku
Článek v odborném periodiku
Obor
30201 Cardiac and Cardiovascular systems
Stát vydavatele
Nizozemské království
Utajení
není předmětem státního či obchodního tajemství
Odkazy
Impakt faktor
Impact factor: 4.600
Kód RIV
RIV/00216224:14310/22:00127632
Organizační jednotka
Přírodovědecká fakulta
UT WoS
000828956200001
Klíčová slova anglicky
FSTL1; FSTL4; FSTL5; Heart failure; Inflammation
Příznaky
Mezinárodní význam, Recenzováno
Změněno: 10. 8. 2023 09:32, Mgr. Marie Šípková, DiS.
Anotace
V originále
Cardiovascular diseases (CVDs) are a group of disorders affecting the heart and blood vessels and a leading cause of death worldwide. Thus, there is a need to identify new cardiokines that may protect the heart from damage as reported in GBD 2017 Causes of Death Collaborators (2018) (The Lancet 392:1736-1788). Follistatin-like 1 (FSTL1) is a cardiokine that is highly expressed in the heart and released to the serum after cardiac injury where it is associated with CVD and predicts poor outcome. The action of FSTL1 likely depends not only on the tissue source but also post-translation modifications that are target tissue- and cell-specific. Animal studies examining the effect of FSTL1 in various models of heart disease have exploded over the past 15 years and primarily report a protective effect spanning from inhibiting inflammation via transforming growth factor, preventing remodeling and fibrosis to promoting angiogenesis and hypertrophy. A better understanding of FSTL1 and its homologs is needed to determine whether this protein could be a useful novel biomarker to predict poor outcome and death and whether it has therapeutic potential. The aim of this review is to provide a comprehensive description of the literature for this family of proteins in order to better understand their role in normal physiology and CVD.
Návaznosti
EF15_003/0000469, projekt VaV |
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EF17_043/0009632, projekt VaV |
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LM2018121, projekt VaV |
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NU22-02-00418, projekt VaV |
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857560, interní kód MU (Kód CEP: EF17_043/0009632) |
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