Publications by authors named "Saidi Jin"

Background: Cardiac hypertrophy is a precursor to heart failure and represents a significant global cause of mortality, thereby necessitating timely and effective therapeutic interventions. Zinc finger protein 36 (Zfp36) is recognised as a critical regulator of ferroptosis; however, its role and underlying mechanisms in cardiac hypertrophy remain largely unexplored. This study aims to investigate the regulatory function of Zfp36 in ferroptosis within the context of cardiac hypertrophy.

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Article Synopsis
  • MicroRNA-15b (miR-15b) and mitofusin-2 (Mfn2) are critical in heart cell death caused by acute myocardial infarction (AMI), with miR-15b elevating and Mfn2 decreasing during ischemic conditions.
  • * The study employed animal and cellular models to show that miR-15b triggers cardiac cell death by inhibiting Mfn2, leading to mitochondrial dysfunction and endoplasmic reticulum (ER) stress, primarily through the PERK/CHOP pathway.
  • * These insights highlight a potential therapeutic target for ischemic heart disease, linking the roles of miR-15b, Mfn2, and apoptotic processes in heart injury.
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  • Cardiac fibrosis is a harmful process leading to heart failure, and this study focuses on a specific circular RNA called circNSD1 and its relationship with the miRNA miR-429-3p in regulating this condition.
  • Researchers created mouse models of heart attack (myocardial infarction) and studied heart cells to observe that miR-429-3p is decreased in cardiac fibrosis, leading to the conclusion that it helps prevent this condition.
  • The study shows that circNSD1 acts as a sponge for miR-429-3p, and reducing circNSD1 may reduce cardiac fibrosis, suggesting circNSD1 could be a new target for treating heart-related diseases.
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The present study was aimed to investigate the effects of circRNA-0028171 on the apoptosis of vascular endothelial cells induced by arsenic trioxide (AsO). Human umbilical vein endothelial cells (HUVECs) were treated with 0-15 μmol/L AsO for 24 h. Then, cellular viability was measured by MTT assay.

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