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Molecular Mechanisms and Treatment Strategies of Myocardial Infarction

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: 30 November 2024 | Viewed by 994

Special Issue Editor


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Guest Editor
National Heart and Lung Institute, Faculty of Medicine, Imperial College London, London SW7 2AZ, UK
Interests: hypertension and hypertensive heart disease; arrhythmias; cardiovascular diseases in women

Special Issue Information

Dear Colleagues,

Myocardial infarction (MI), like all other atherosclerotic diseases, carries multifactorial pathological mechanisms, the majority of which are modifiable. However, there remains an important cause of MI, namely molecular genetical factors. Several studies have shown chromosomal linkage to MI. Certainly, in such cases, a molecular mechanism will play a big role. Subsequently, since there is a molecular mechanism, a question will arise as to whether there are ways to prevent such mechanisms from occurring and treat the disease. There should be a great advantage to studying this approach and promoting research to apply it to treating MI.

This Special Issue will collect research articles and comprehensive reviews that delve into the intricate molecular pathology of, as well as innovative molecular therapeutic strategies for, myocardial infarction.

Dr. Abdul Majeed Salmasi
Guest Editor

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Keywords

  • myocardial infarction
  • genetics
  • molecular biology
  • chromosomes
  • genes
  • atherosclerosis
  • coronary artery disease
  • risk factors

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Published Papers (1 paper)

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Research

16 pages, 3164 KiB  
Article
The Beneficial Effect of the SGLT2 Inhibitor Dapagliflozin in Alleviating Acute Myocardial Infarction-Induced Cardiomyocyte Injury by Increasing the Sirtuin Family SIRT1/SIRT3 and Cascade Signaling
by Yi-Hsiung Lin, Wei-Chung Tsai, Chien-Chih Chiu, Nai-Yu Chi, Yi-Hsueh Liu, Tien-Chi Huang, Wei-Tsung Wu, Tsung-Hsien Lin, Wen-Ter Lai, Sheng-Hsiung Sheu and Po-Chao Hsu
Int. J. Mol. Sci. 2024, 25(15), 8541; https://doi.org/10.3390/ijms25158541 - 5 Aug 2024
Viewed by 831
Abstract
Sodium-glucose cotransporter-2 inhibitors (SGLT2i) have a variety of cardiovascular and renoprotective effects and have been developed as novel agents for the treatment of heart failure. However, the beneficial mechanisms of SGLT2i on cardiac tissue need to be investigated further. In this study, we [...] Read more.
Sodium-glucose cotransporter-2 inhibitors (SGLT2i) have a variety of cardiovascular and renoprotective effects and have been developed as novel agents for the treatment of heart failure. However, the beneficial mechanisms of SGLT2i on cardiac tissue need to be investigated further. In this study, we established a mouse model of acute myocardial infarction (AMI) using coronary artery constriction surgery and investigated the role of dapagliflozin (DAPA) in protecting cardiomyocytes from hypoxic injury induced by AMI. In vitro experiments were done using hypoxic cultured H9c2 ventricular cells to verify this potential mechanism. Expression of the SIRT family and related genes and proteins was verified by qPCR, Western blotting and immunofluorescence staining, and the intrinsic potential mechanism of cardiomyocyte death due to AMI and hypoxia was comprehensively investigated by RNA sequencing. The RNA sequencing results of cardiomyocytes from AMI mice showed that the SIRT family may be mainly involved in the mechanisms of hypoxia-induced cardiomyocyte death. In vitro hypoxia-induced ventricular cells showed the role of dapagliflozin in conferring resistance to hypoxic injury in cardiomyocytes. It showed that SIRT1/3/6 were downregulated in H9c2 cells in a hypoxic environment, and the addition of dapagliflozin significantly increased the gene and protein expression of SIRT1, 3 and 6. We then verified the underlying mechanisms induced by dapagliflozin in hypoxic cardiomyocytes using RNA-seq, and found that dapagliflozin upregulated the hypoxia-induced gene downregulation, which includes ESRRA, EPAS1, AGTRAP, etc., that associated with SIRTs-related and apoptosis-related signaling to prevent H9c2 cell death. This study provides laboratory data for SGLT2i dapagliflozin treatment of AMI and confirms that dapagliflozin can be used to treat hypoxia-induced cellular necrosis in cardiomyocytes, in which SIRT1 and SIRT3 may play an important role. This opens up further opportunities for SGLT2i in the treatment of heart disease. Full article
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