[Retracted] Activating autophagy and ferroptosis of 3‑Chloropropane‑1,2‑diol induces injury of human umbilical vein endothelial cells via AMPK/mTOR/ULK1.

Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that the flow cytometric assay data shown in Fig. 2C on p. 5, certain of the fluorescence microscopy data shown in Fig.

Paeonol improves angiotensin II-induced cardiac hypertrophy by suppressing ferroptosis.

The aim of this study was to investigate the protective effect of paeonol (pae) on an angiotensin II (AngII)-induced cardiac hypertrophy mouse model. First, AngII mouse models were constructed and randomly grouped into the control (con), AngII, and AngII + Pae groups. Compared with that in the blank group, the surface area of myocardial cells in the AngII group increased significantly.

Activating autophagy and ferroptosis of 3‑Chloropropane‑1,2‑diol induces injury of human umbilical vein endothelial cells via AMPK/mTOR/ULK1.

3‑Chloropropane‑1,2‑diol (3‑MCPD) is an internationally recognized food pollutant. 3‑MCPD has reproductive, renal and neurotoxic properties. However, whether 3‑MCPD induces human umbilical vein endothelial cell (HUVEC) injury has not been previously reported.

Decreased miR-208 induced ischemia myocardial and reperfusion injury by targeting p21.

Aberrant expression of miR-208 was previously reported in cardiomyocytes after cardiac ischemia reperfusion (CIR) injury. However, the underlying mechanism has never been elucidated. In the current study, the relative level of miR-208 was determined in the hearts of CIR injury mice models using real time PCR.