C
Chun-Yan Kong
Researcher at Wuhan University
Publications - 19
Citations - 879
Chun-Yan Kong is an academic researcher from Wuhan University. The author has contributed to research in topics: Cardiac fibrosis & Cardiotoxicity. The author has an hindex of 11, co-authored 15 publications receiving 403 citations.
Papers
More filters
Journal ArticleDOI
FNDC5 alleviates oxidative stress and cardiomyocyte apoptosis in doxorubicin-induced cardiotoxicity via activating AKT.
Xin Zhang,Can Hu,Chun-Yan Kong,Peng Song,Hai-Ming Wu,Si-Chi Xu,Yu-Pei Yuan,Wei Deng,Zhen-Guo Ma,Qi-Zhu Tang +9 more
TL;DR: Mechanistically, it was identified that FNDC5/Irisin activated AKT/mTOR signaling and decreased DOX-induced cardiomyocyte apoptosis, and moreover, direct evidence was provided that the anti-oxidant effect of F NDC5 / irisin was mediated by the AKT /GSK3β/FYN/Nrf2 axis in an mTOR-independent manner.
Journal ArticleDOI
Meteorin-like protein attenuates doxorubicin-induced cardiotoxicity via activating cAMP/PKA/SIRT1 pathway.
Can Hu,Xin Zhang,Peng Song,Yu-Pei Yuan,Chun-Yan Kong,Hai-Ming Wu,Si-Chi Xu,Zhen-Guo Ma,Qi-Zhu Tang +8 more
TL;DR: Cardiac-derived METRNL activates SIRT1 via cAMP/PKA signaling axis in an autocrine manner, which ultimately improves DOX-elicited oxidative stress, apoptosis and cardiac dysfunction, which may provide a novel therapeutic strategy for the prevention ofDOX-associated cardiotoxicity.
Journal ArticleDOI
Rosmarinic acid attenuates cardiac fibrosis following long-term pressure overload via AMPKα/Smad3 signaling
Xin Zhang,Zhen-Guo Ma,Yu-Pei Yuan,Si-Chi Xu,Wen-Ying Wei,Peng Song,Chun-Yan Kong,Wei Deng,Qi-Zhu Tang +8 more
TL;DR: RA attenuated cardiac fibrosis following long-term pressure overload via AMPKα/Smad3 signaling and PPAR-γ was required for the activation of AMPK α and abolished RA-mediated protective effects in vitro.
Journal ArticleDOI
Rosmarinic acid alleviates cardiomyocyte apoptosis via cardiac fibroblast in doxorubicin-induced cardiotoxicity.
Xin Zhang,Jin-Xiu Zhu,Zhen-Guo Ma,Hai-Ming Wu,Si-Chi Xu,Peng Song,Chun-Yan Kong,Yu-Pei Yuan,Wei Deng,Qi-Zhu Tang +9 more
TL;DR: RA alleviated DOX-induced cardiomyocyte apoptosis by inhibiting the expression and release of Fas L in CFs via a paracrine manner, moreover, NFAT as well as MMP7 inhibition were responsible for the suppression of FasL.
Journal ArticleDOI
C1q-tumour necrosis factor-related protein-3 exacerbates cardiac hypertrophy in mice.
TL;DR: It is suggested that CTRP3 promotes pressure overload-induced cardiac hypertrophy via activation of the TAK1-JNK axis and loses its pro-hypertrophic effects in cardiomyocyte-specific Tak1 knockout mice.