基于内质网应激和自噬探讨H2S在脓毒症心肌损伤炎症反应中的作用及机制
序号 | 标题 | 类型 | 作者 |
---|---|---|---|
1 | H2S attenuates sepsis‑induced cardiac dysfunction via a PI3K/Akt‑dependent mechanism | 期刊论文 | Jian-Ping Liu;Jianhua Li;Peigang Tian;Bahaer Guli;Guopeng Weng;L I Li;Qinghong Cheng |
2 | Sepsis causes heart injury through endoplasmic reticulum stress-mediated apoptosis signaling pathway | 期刊论文 | Li Lei;Peng Xin;Guo Lichun;Zhao Yuhan;Cheng Qinghong |
3 | H2S regulation of ferroptosis attenuates sepsis‑induced cardiomyopathy | 期刊论文 | Guodong Cao;Youcheng Zeng;Yuhan Zhao;Liang Lin;Xiqing Luo;Lichun Guo;Yixin Zhang;Qinghong Cheng |
4 | H2S通过调节铁死亡中Xc-/GPX4通路减轻脓毒症心肌损伤 | 期刊论文 | Guodong Cao;Qinghong Cheng |
5 | NCOA4介导的铁蛋白自噬参与LPS诱导的心肌细胞铁死亡 | 期刊论文 | Lichun Guo;Qinghong Cheng |
6 | Exogenous H2S Protects against Septic Cardiomyopathy by Inhibiting Autophagy through the AMPK/mTOR Pathway | 期刊论文 | YuHan Zhao;QingHong Cheng |
7 | 硫化氢通过抑制ROS介导的内质网应激改善脓毒症心肌损伤的研究 | 期刊论文 | Yuhan Zhao;Qinghong Cheng |
8 | 白藜芦醇对大鼠脓毒症心肌病铁死亡的影响及机制 | 期刊论文 | Youcheng Zeng;Qinghong Cheng |