Acute myocardial infarction

Reed, Grant W.; Rossi, Jeffrey E.; Cannon, Christopher P.

doi:10.1016/s0140-6736(16)30677-8

Cited by 1,011 publications

(765 citation statements)

References 139 publications

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“…Acute myocardial infarction (AMI) is one of the most severe manifestations of coronary artery diseases that causes irreversible damage to the heart muscle, and can lead to development of heart failure [1, 2]. AMI leads to more than 4 million deaths in Europe and northern Asia [3].…”

Section: Introductionmentioning

confidence: 99%

Long Non-Coding RNA H19 Protects H9c2 Cells against Hypoxia-Induced Injury by Targeting MicroRNA-139

Gong¹,

Xu²,

Guo³

et al. 2017

Cell Physiol Biochem

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Background/Aims: Acute myocardial infarction (AMI) occurs when blood supply to the heart is diminished (ischemia) for long time; ischemia is primarily caused due to hypoxia. The present study evaluated the effects of long non-coding RNA H19 on hypoxic rat H9c2 cells and mouse HL-1 cells. Methods: Hypoxic injury was confirmed by measuring cell viability, migration and invasion, and apoptosis using MTT, Transwell and flow cytometry assays, respectively. H19 expression after hypoxia was estimated by qRT-PCR. We then measured the effects of non-physiologically expressed H19, knockdown of miR-139 with or without H19 silence, and abnormally expressed Sox8 on hypoxia-induced H9c2 cells. Moreover, the interacted miRNA for H19 and downstream target gene were virtually screened and verified. The involved signaling pathways and the effects of abnormally expressed H19 on contractility of HL-1 cells were explored via Western blot analysis. Results: Hypoxia induced decreases of cell viability, migration and invasion, increase of cell apoptosis and up-regulation of H19. Knockdown of H19 increased hypoxia-induced injury in H9c2 cells. H19 acted as a sponge for miR-139 and H19 knockdown aggravated hypoxia-induced injury by up-regulating miR-139. Sox8 was identified as a target of miR-139, and its expression was negatively regulated by miR-139. The mechanistic studies revealed that overexpression of Sox8 might decrease hypoxia-induced cell injury by activating the PI3K/AKT/mTOR pathway and MAPK. Besides, H19 promoted contractility of HL-1 cells. Conclusion: These findings suggest that H19 alleviates hypoxia-induced myocardial cell injury by miR-139-mediated up-regulation of Sox8, along with activation of the PI3K/AKT/mTOR pathway and MAPK.

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Section: Introductionmentioning

confidence: 99%

Long Non-Coding RNA H19 Protects H9c2 Cells against Hypoxia-Induced Injury by Targeting MicroRNA-139

Gong¹,

Xu²,

Guo³

et al. 2017

Cell Physiol Biochem

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“…Recent advances in the treatment of ST‐segment–elevation myocardial infarction (STEMI) have resulted in improved outcomes over the past 2 decades 1, 2. However, STEMI remains a significant cause of morbidity and mortality in the United States.…”

Section: Introductionmentioning

confidence: 99%

Thirty‐Day Readmission Rates, Timing, Causes, and Costs after ST‐Segment–Elevation Myocardial Infarction in the United States: A National Readmission Database Analysis 2010–2014

Kim

Yeo

Cheung

et al. 2018

JAHA

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BackgroundReadmission after ST‐segment–elevation myocardial infarction (STEMI) poses an enormous economic burden to the US healthcare system. Efforts to prevent readmissions should be based on understanding the timing and causes of these readmissions. This study aimed to investigate contemporary causes, timing, and cost of 30‐day readmissions after STEMI.Methods and ResultsAll STEMI hospitalizations were selected in the Nationwide Readmissions Database (NRD) from 2010 to 2014. The 30‐day readmission rate as well as the primary cause and cost of readmission were examined. Multivariate regression analysis was performed to identify the predictors of 30‐day readmission and increased cumulative cost. From 2010 to 2014, the 30‐day readmission rate after STEMI was 12.3%. Within 7 days of discharge, 43.9% were readmitted, and 67.3% were readmitted within 14 days. The annual rate of 30‐day readmission decreased by 19% from 2010 to 2014 (P<0.001). Female sex, AIDS, anemia, chronic kidney disease, collagen vascular disease, diabetes mellitus, hypertension, pulmonary hypertension, congestive heart failure, atrial fibrillation, and increased length of stay were independent predictors of 30‐day readmission. A large proportion of patients (41.6%) were readmitted for noncardiac reasons. After multivariate adjustment, 30‐day readmission was associated with a 47.9% increase in cumulative cost (P<0.001).ConclusionsTwo thirds of patients were readmitted within the first 14 days after STEMI, and a large proportion of patients were readmitted for noncardiac reasons. Thirty‐day readmission was associated with an ≈50% increase in cumulative hospitalization costs. These findings highlight the importance of closer surveillance of both cardiac and general medical conditions in the first several weeks after STEMI discharge.

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“…Myocardial ischemia/reperfusion injury is one of the most common causes of death worldwide [1][2][3][4][5][6]. Numerous studies have demonstrated that cell death is an important component in the pathogenesis of various cardiac diseases, including heart failure, myocardial infarction (MI) and ischemia/reperfusion (I/R) [7][8][9][10].…”

Section: Introductionmentioning

confidence: 99%

FGF-2 Transcriptionally Down-Regulates the Expression of BNIP3L via PI3K/Akt/FoxO3a Signaling and Inhibits Necrosis and Mitochondrial Dysfunction Induced by High Concentrations of Hydrogen Peroxide in H9c2 Cells

Chen

Han

et al. 2016

Cell Physiol Biochem

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Background/Aims: Cardiovascular disease is a growing major global public health problem. Necrosis is one of the main forms of cardiomyocyte death in heart disease. Oxidative stress is regarded as one of the key regulators of cardiac necrosis, which eventually leads to cardiovascular disease. Many pharmacological and in vitro studies have suggested that FGF-2 can act directly on cardiomyocytes to maintain the integrity and function of the myocardium and prevent damage during oxidative stress. However, the mechanisms by which FGF-2 rescues the myocardium from oxidative stress damage in cardiovascular disease remain unclear. The present study explored the protective effects of FGF-2 in the H₂O₂-induced necrosis of H9C2 cardiomyocytes as well as the possible signaling pathways involved. Methods: Necrosis of H9c2 cardiomyocytes was induced by H₂O₂ and assessed using a Cell Counting Kit-8 (CCK8) assay and flow cytometry analysis. The cells were pretreated with the PI3K/Akt inhibitor Wortmannin to investigate the possible involvement of the PI3K/Akt pathway in the protection by FGF-2. The levels of Akt, p-Akt, FoxO3a, p-FoxO3a, and BNIP3L were detected by Western blot. Chromatin immuno-precipitation (ChIP) analysis was used to test whether FoxO3a binds directly to the BNIP3L promoter region. A luciferase assay was used to study the effects of FoxO3a on BNIP3L gene promoter activity. Mitochondrial ΔΨM was quantified using tetramethylrhodamine methyl ester perchlorate (TMRM). The mitochondrial oxygen consumption rate (OCR) was assessed with a Seahorse XF24 Analyzer. Results: Treatment with H₂O₂ decreased the phosphorylation of Akt and FoxO3a, and it induced the nuclear localization of FoxO3a and the necrosis of H9c2 cells. These effects of H₂O₂ were abrogated by pretreatment with FGF-2. Furthermore, the protective effects of FGF-2 were abolished by the PI3K/Akt inhibitor Wortmannin. ChIP analyses indicated that FoxO3a binds directly to the BNIP3L promoter region. Using a luciferase assay, we further observed that FoxO3a increased BNIP3L gene promoter activity. As expected, overexpression of BNIP3L in H9C2 cardiomyoblast cells reduced the cardioprotection of FGF-2 in H₂O₂-induced necrosis and mitochondrial dysfunction. Conclusions: The present data suggest that FGF-2 protects against H₂O₂-induced necrosis of H9C2 cardiomyocytes via the activation of the PI3K/Akt/FoxO3a pathway. Moreover, the present results demonstrate that FoxO3a is an important transcription factor that acts by binding to the promoter and promoting the transcription of BNIP3L, and it contributes to the necrosis and mitochondrial dysfunction induced by H₂O₂ in H9c2 cardiomyoblast cells.

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Acute myocardial infarction

Cited by 1,011 publications

References 139 publications

Long Non-Coding RNA H19 Protects H9c2 Cells against Hypoxia-Induced Injury by Targeting MicroRNA-139

Long Non-Coding RNA H19 Protects H9c2 Cells against Hypoxia-Induced Injury by Targeting MicroRNA-139

Thirty‐Day Readmission Rates, Timing, Causes, and Costs after ST‐Segment–Elevation Myocardial Infarction in the United States: A National Readmission Database Analysis 2010–2014

FGF-2 Transcriptionally Down-Regulates the Expression of BNIP3L via PI3K/Akt/FoxO3a Signaling and Inhibits Necrosis and Mitochondrial Dysfunction Induced by High Concentrations of Hydrogen Peroxide in H9c2 Cells

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