Emodin alleviates cardiac fibrosis by suppressing activation of cardiac fibroblasts
Angiotensin II
Cardiac fibroblast
Cardiac fibrosis
Emodin
MTA3
Mouse
Journal
Acta pharmaceutica Sinica. B
ISSN: 2211-3835
Titre abrégé: Acta Pharm Sin B
Pays: Netherlands
ID NLM: 101600560
Informations de publication
Date de publication:
Jul 2019
Jul 2019
Historique:
received:
13
11
2018
revised:
21
03
2019
accepted:
02
04
2019
entrez:
7
8
2019
pubmed:
7
8
2019
medline:
7
8
2019
Statut:
ppublish
Résumé
Excess activation of cardiac fibroblasts inevitably induces cardiac fibrosis. Emodin has been used as a natural medicine against several chronic diseases. The objective of this study is to determine the effects of emodin on cardiac fibrosis and the underlying molecular mechanisms. Intragastric administration of emodin markedly decreased left ventricular wall thickness in a mouse model of pathological cardiac hypertrophy with excess fibrosis induced by transaortic constriction (TAC) and suppressed activation of cardiac fibroblasts induced by angiotensin II (AngII). Emodin upregulated expression of metastasis associated protein 3 (MTA3) and restored the MTA3 expression in the setting of cardiac fibrosis. Moreover, overexpression of MTA3 promoted cardiac fibrosis; in contrast, silence of MTA3 abrogated the inhibitory effect of emodin on fibroblast activation. Our findings unraveled the potential of emodin to alleviate cardiac fibrosis
Identifiants
pubmed: 31384533
doi: 10.1016/j.apsb.2019.04.003
pii: S2211-3835(18)31132-8
pmc: PMC6664101
doi:
Types de publication
Journal Article
Langues
eng
Pagination
724-733Références
Chin Med J (Engl). 2006 May 20;119(10):868-70
pubmed: 16732991
Tohoku J Exp Med. 2012;227(3):225-30
pubmed: 22791134
Oncol Rep. 2012 Dec;28(6):1991-6
pubmed: 22992976
J Invest Dermatol. 2013 Jun;133(6):1646-54
pubmed: 23340735
Cardiovasc Diabetol. 2013 Feb 23;12:36
pubmed: 23432808
Cell Mol Life Sci. 2014 Feb;71(4):549-74
pubmed: 23649149
PLoS One. 2013 May 03;8(5):e62986
pubmed: 23671646
Rheumatology (Oxford). 2013 Sep;52(9):1583-91
pubmed: 23685361
J Mol Cell Cardiol. 2014 May;70:47-55
pubmed: 24625635
J Pharmacol Exp Ther. 2014 Jun;349(3):417-26
pubmed: 24676878
Pharmazie. 2014 May;69(5):374-8
pubmed: 24855831
Br J Pharmacol. 2015 Dec;172(23):5559-72
pubmed: 25362897
Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi. 2015 Mar;31(3):350-4
pubmed: 25744842
Cell Physiol Biochem. 2015;36(4):1517-26
pubmed: 26159184
Chem Biol Interact. 2015 Dec 5;242:99-106
pubmed: 26428355
J Cell Mol Med. 2016 Mar;20(3):495-505
pubmed: 26756969
Metabolism. 2016 Feb;65(2):30-40
pubmed: 26773927
Curr Protein Pept Sci. 2016;17(8):726-734
pubmed: 27033852
Cell Physiol Biochem. 2016;38(6):2103-22
pubmed: 27184887
Phytother Res. 2016 Aug;30(8):1207-18
pubmed: 27188216
Circ Res. 2016 Sep 30;119(8):909-20
pubmed: 27502479
Adv Exp Med Biol. 2016;928:47-73
pubmed: 27671812
Sci Rep. 2016 Oct 10;6:34284
pubmed: 27721485
Mol Med Rep. 2016 Nov;14(5):4643-4649
pubmed: 27748907
Sci Rep. 2016 Oct 24;6:35696
pubmed: 27774992
J Cell Mol Med. 2017 Apr;21(4):758-767
pubmed: 27878946
Sheng Li Xue Bao. 2016 Dec 25;68(6):747-756
pubmed: 28004069
Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi. 2017 Jan;33(1):67-71
pubmed: 28031118
Chin J Cancer. 2017 Mar 9;36(1):28
pubmed: 28279208
Tumour Biol. 2017 Mar;39(3):1010428317695027
pubmed: 28351306
AIMS Med Sci. 2017;4(1):17-27
pubmed: 28959722
Oncotarget. 2017 Jun 27;8(38):63084-63095
pubmed: 28968973
Sci Rep. 2018 Jun 18;8(1):9302
pubmed: 29915390
Biochem Biophys Res Commun. 2018 Sep 10;503(3):1625-1632
pubmed: 30041821
Int Heart J. 2018 Sep 26;59(5):1123-1133
pubmed: 30101852
Eur J Pharmacol. 2018 Nov 5;838:170-176
pubmed: 30170066
Biochem Biophys Res Commun. 2018 Nov 10;505(4):973-978
pubmed: 30274778
Int J Neuropsychopharmacol. 2019 Jan 1;22(1):57-70
pubmed: 30407508
Front Pharmacol. 2018 Nov 19;9:1328
pubmed: 30510513