Asset Details
Do you wish to reserve the book?
Pyroptosis inhibition improves the symptom of acute myocardial infarction
Hey, we have placed the reservation for you!
By the way, why not check out events that you can attend while you pick your title.
Oops! Something went wrong.
Looks like we were not able to place the reservation. Kindly try again later.
Are you sure you want to remove the book from the shelf?
Pyroptosis inhibition improves the symptom of acute myocardial infarction
Do you wish to request the book?
Pyroptosis inhibition improves the symptom of acute myocardial infarction
Please be aware that the book you have requested cannot be checked out. If you would like to checkout this book, you can reserve another copy
We have requested the book for you!
Your request is successful and it will be processed during the Library working hours. Please check the status of your request in My Requests.
Oops! Something went wrong.
Looks like we were not able to place your request. Kindly try again later.
Journal Article
Pyroptosis inhibition improves the symptom of acute myocardial infarction
2021
Overview
Acute myocardial infarction (AMI), the leading cause of mortality worldwide, is a rapidly developing and irreversible disease. Therefore, proper prompt intervention at the early stage of AMI is crucial for its treatment. However, the molecular features in the early stage have not been clarified. Here, we constructed mouse AMI model and profiled transcriptomes and proteomes at the early stages of AMI progress. Immune system was extensively activated at 6-h AMI. Then, pyroptosis was activated at 24-h AMI. VX-765 treatment, a pyroptosis inhibitor, significantly reduced the infarct size and improved the function of cardiomyocytes. Besides, we identified that WIPI1, specifically expressed in heart, was significantly upregulated at 1 h after AMI. Moreover,
WIPI1
expression is significantly higher in the peripheral blood of patients with AMI than healthy control. WIPI1 can serve as a potential early diagnostic biomarker for AMI. It likely decelerates AMI progress by activating autophagy pathways. These findings shed new light on gene expression dynamics in AMI progress, and present a potential early diagnostic marker and a candidate drug for clinical pre-treatment to prolong the optimal cure time.
Publisher
Nature Publishing Group UK,Springer Nature B.V,Nature Publishing Group
Subject
/ 38
/ 38/47
/ Animals
/ Autophagy-Related Proteins - metabolism
/ Biomedical and Life Sciences
/ Gene Expression Regulation - drug effects
/ Male
/ Mice
/ Myocardial Infarction - diagnosis
/ Myocardial Infarction - genetics
/ Myocardial Infarction - pathology
/ para-Aminobenzoates - pharmacology
/ Signal Transduction - drug effects
/ Signal Transduction - genetics
