Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8294741 | PMC |
| http://dx.doi.org/10.36660/abc.20210500 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
[Mechanism of ginsenoside Rg_1 in regulating autophagy through miR-155/Notch1/Hes1 pathway to attenuate hypoxia/reoxygenation injury in HL-1 cells].
Zhongguo Zhong Yao Za Zhi
December 2024
School of Traditional Chinese Medicine, Binzhou Medical College Yantai 264003, China Institute of Basic Medicine, Xiyuan Hospital, China Academy of Chinese Medical Sciences Beijing 100091, China.
This article explored the specific mechanism by which ginsenoside Rg_1 regulates cellular autophagy to attenuate hypoxia/reoxygenation(H/R) injury in HL-1 cardiomyocytes through the microRNA155(miR-155)/neurogenic gene Notch homologous protein 1(Notch1)/hairy and enhancer of split 1(Hes1) pathway. An HL-1 cell model with H/R injury was constructed, and ginsenoside Rg_1 and/or Notch1 inhibitor DAPT and miR-155 mimics were used to treat cells. Cell counting kit(CCK)-8 was used to detect the relative viability of HL-1 cells with H/R injury.
View Article and Find Full Text PDFCardiac-targeted delivery of a novel Drp1 inhibitor for acute cardioprotection.
J Mol Cell Cardiol Plus
September 2024
O'Brien Institute Department, St Vincent's Institute of Medical Research, Victoria 3065, Australia.
Dynamin-related protein 1 (Drp1) is a mitochondrial fission protein and a viable target for cardioprotection against myocardial ischaemia-reperfusion injury. Here, we reported a novel Drp1 inhibitor (DRP1i1), delivered using a cardiac-targeted nanoparticle drug delivery system, as a more effective approach for achieving acute cardioprotection. DRP1i1 was encapsulated in cubosome nanoparticles with conjugated cardiac-homing peptides (NanoDRP1i1) and the encapsulation efficiency was 99.
View Article and Find Full Text PDFSpontaneous coronary artery dissection (SCAD) is characterized by intramural hematoma in a coronary artery leading to partial or complete vessel obstruction. A 51-year-old female was hospitalized with acute myocardial infarction and cardiogenic shock. She was diagnosed with severe SCAD, affecting the proximal left coronary artery.
View Article and Find Full Text PDFCirculating autophagy regulator Rubicon is linked to increased myocardial infarction risk.
J Mol Cell Cardiol Plus
March 2025
Center for Clinical Investigation (CIC1436)/CARDIOMET, Rangueil University Hospital, Toulouse, France.
Background: The identification of new biomarkers that improve existing cardiovascular risk prediction models for acute coronary syndrome is essential for accurately identifying high-risk patients and refining treatment strategies. Autophagy, a vital cellular degradation mechanism, is important for maintaining cardiac health. Dysregulation of autophagy has been described in cardiovascular conditions such as myocardial ischemia-reperfusion injury, a key factor in myocardial infarction (MI).
View Article and Find Full Text PDFClinical Review of Cardiogenic Shock After Acute Myocardial Infarction - Revascularization, Mechanical Circulatory Support, and Beyond.
Circ Rep
January 2025
Department of Cardiovascular Medicine, Chiba University Graduate School of Medicine Chiba Japan.
Owing to recent advances in early reperfusion and pharmacological therapies, the prognosis of patients with acute myocardial infarction (AMI) has considerably improved over the past decades. However, the mortality rate remains high at ~40-50% after AMI when complicated by cardiogenic shock. Although immediate coronary revascularization of the infarct-related artery has been the only evidence-based treatment, temporary mechanical circulatory support with a microaxial flow pump (Impella) has become another therapeutic option supported by randomized trial data in highly selected patients.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!