State-of-the-art diagnosis of myocardial infarction

Vafaie, Mehrshad

doi:10.1515/dx-2016-0024

Cited by 32 publications

(36 citation statements)

References 28 publications

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“…Damage of cardiomyocytes caused by acute and persistent hypoxia has been found to play key roles in the occurrence and development of MI 1,22 . Herein, we revealed that SF I, a flavonoid extracted from the root of Scutellaria baicalensis , could mitigate rat embryonic ventricular myocardium-derived H9c2 cell and primary cardiomyocytes proliferation inhibition and apoptosis caused by hypoxia.…”

Section: Discussionmentioning

confidence: 99%

“…Myocardial infarction (MI) is a serious heart disease in which blood perfusion to the heart is reduced, resulting in decreased oxygen supplement to cardiomyocytes. 1,2 It is the most common reason for sudden death and characterized by massive cardiomyocytes damage and apoptosis. 3 Moreover, the damaged cardiomyocytes will be replaced by fibrous tissue after MI, which cannot carry out normal functions of cardiomyocytes and contributes to the formation and development of chronic ischemic heart diseases.…”

Section: Introductionmentioning

confidence: 99%

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RETRACTED: Skullcapflavone I protects cardiomyocytes from hypoxia-caused injury through up-regulation of lincRNA-ROR

Zhang

et al. 2019

Int J Immunopathol Pharmacol

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Myocardial infarction (MI) is a serious heart disease in which cardiomyocytes are damaged, caused by hypoxia. This study explored the possible protective activity of Skullcapflavone I (SF I), a flavonoid isolated from the root of Scutellaria baicalensis Georgi, on hypoxia-stimulated cardiomyocytes cell injury in vitro. Viability and apoptosis of H9c2 cells and primary cardiomyocytes were tested using cell counting kit-8 (CCK-8) assay and Guava Nexin Reagent, respectively. Quantitative reverse transcription polymerase chain reaction (qRT-PCR) was used to measure the long non-coding RNA regulator of reprogramming (lincRNA-ROR) expression. si-ROR was transfected to knockdown lincRNA-ROR. Western blotting was conducted to assess the protein levels of key molecules related to cell proliferation, apoptosis, and mitogen-activated protein kinase/extracellular signal-regulated kinase (MEK/ERK) pathway. We discovered that hypoxia stimulation obviously reduced H9c2 cell and primary cardiomyocytes' viability and proliferation, but promoted cell apoptosis. SF I treatment mitigated the cell viability and proliferation inhibition, as well as cell apoptosis caused by hypoxia. Moreover, SF I promoted the hypoxia-caused up-regulation of lincRNA-ROR in H9c2 cells and primary cardiomyocytes. Knockdown of lincRNA-ROR reversed the influence of SF I on hypoxia-stimulated H9c2 cells and primary cardiomyocytes. Besides, SF I activated MEK/ERK pathway in H9c2 cells and primary cardiomyocytes via upregulating lincRNA-ROR. To sum up, our research verified the beneficial activity of SF I on hypoxia-caused cardiomyocytes injury. SF I protected cardiomyocytes from hypoxia-caused injury through up-regulation of lincRNA-ROR and activation of MEK/ERK pathway.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

RETRACTED: Skullcapflavone I protects cardiomyocytes from hypoxia-caused injury through up-regulation of lincRNA-ROR

Zhang

et al. 2019

Int J Immunopathol Pharmacol

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“…Most of the MI occurs due to coronary artery disease and the risk factors include hypertension, family history, smoking, diabetes, obesity, hyperlipidemia, and so on . Usually, the complete blocking of a coronary arteries by atherosclerotic plaque rupture is the potential mechanism . However, the detailed mechanism for the occurrence of MI is still under investigation.…”

Section: Introductionmentioning

confidence: 99%

“…3 Usually, the complete blocking of a coronary arteries by atherosclerotic plaque rupture is the potential mechanism. 3,5 However, the detailed mechanism for the occurrence of MI is still under investigation.…”

Section: Introductionmentioning

confidence: 99%

lncRNA GAS5 regulates myocardial infarction by targeting the miR‐525‐5p/CALM2 axis

Zhang

Hou

Gao

et al. 2019

J of Cellular Biochemistry

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Long noncoding RNAs (lncRNAs) play critical roles in the pathogenesis of cardiovascular diseases, especially in myocardial infarction (MI). However, the underlying molecular mechanism of how lncRNA involves and affect MI still remains unclear. This study aimed to investigate the expression of lncRNA growth arrest‐specific transcript 5 (GAS5) and its effects on myocardial cells' proliferation, cell cycle, and apoptosis. The possible mechanisms involved in GAS5, calmodulin 2 (CALM2), and microRNA (miR)‐525‐5p were also explored. The messenger RNA (mRNA) level of CALM2, GAS5, and miR‐525‐5p in postmyocardial infarction (MI) and normal cells were examined by quantitative real‐time polymerase chain reaction (RT‐qPCR). Western blot analysis assay was conducted to detect the protein levels of CALM2. The changes of cell cycle/apoptosis and cell viability of post‐MI myocardial cells (PMMC) were determined by flow cytometry analysis and MTT (3‐(4,5‐dimethyl‐2‐thiazolyl)‐2,5‐diphenyl‐2H‐tetrazolium bromide) assay after knockdown of GAS5 or CALM2, respectively. Dual luciferase reporter assay and RNA‐binding protein immunoprecipitation (RIP) assay were performed to verify the targeting relationship between miR‐525‐5p and GAS5, CALM2 in myocardial. Hypoxic preconditioning was performed in normal cells, which constructed a simulated MI environment, and the effect of GAS5 on cardiomyocyte apoptosis was detected. Our data showed that the expression of GAS5 and CALM2 in PMMC was significantly upregulated, while the expression of miR‐525‐5p was downregulated. Overexpression of GAS5 and CALM2 profoundly promoted the apoptosis of myocardial cell. However, the proliferation of myocardial cell was inhibited by the upregulation of GAS5 and CALM2. Moreover, GAS5 was proved to be the target of miR‐525‐5p and GAS5 downregulated the expression of miR‐525‐5p and CALM2. In addition, lncRNA GAS5 promotes MI, while CALM2 induced MI can be reversed by miR‐525‐5p. These data suggested that lncRNA GAS5 promoted the development and progression of MI via targeting of the miR‐525‐5p/CALM2 axis and it has the potential to be explored as a therapeutic target for the treatment of MI in the future.

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“…Among all currently known laboratory biomarkers of AMI, 10,24,[29][30][31] cardiac troponins remain the most demanded ones in clinical practice; however, they are not devoid of several disadvantages, among which the following ones are worth mentioning: 1) relatively late time of establishing the fact of cardiomyocyte damage or death, 2) insufficient specificity in relation to ischemic necrosis of cardiomyocytes in AMI, and this is manifested by the fact that at the early stages of examination it is almost impossible to establish the cause and mechanism of cardiac muscle damage, which is key to making a correct diagnosis, 3) lack of standardization of existing methods of determination, which is expressed by the fact that diagnostic tests of different manufacturers, having different analytical characteristics, give different results in samples received from the same patient, and in some cases, in particular during transportation or transfer of patients to another hospital, that does not allow to assess dynamic changes of cTnI and cTnT levels.…”

Section: Cardiac-specific Troponins (Ctni and Ctnt) As Laboratory Biomarkers Of Myocardial Injury: Practical Application Possibilitiesmentioning

confidence: 99%

Cardiac Troponins: Contemporary Biological Data and New Methods of Determination

Chaulin¹

2021

VHRM

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Laboratory diagnosis plays one of the key roles in the diagnosis of many diseases, including cardiovascular diseases (CVD). The methods underlying the in vitro study of many CVD biomarkers, including cardiac troponins (cTnI and cTnT), are imperfect and are continually being improved to enhance their analytical performance, with sensitivity and specificity being the most important. Recently developed improved cTnI and cTnT detection methods, referred to as highly sensitive methods (hs-cTnI, hs-cTnT), have changed many of our ideas about the biology of cardiac troponins and opened up a number of additional diagnostic capabilities for practical healthcare. This article systematizes some relevant data on the biology of cardiac troponins as well as on methods for determining cTnI and cTnT with an analysis of the diagnostic value of their analytical characteristics (limit of blank, limit of detection, 99th percentile, coefficient of variation, and others). Data on extracardiac expression of cTnI and cTnT, mechanisms of formation and potential clinical significance of gender, age, and circadian characteristics of hs-cTnI and hs-cTnT content in serum are discussed. Considerable attention is paid to the discussion of new diagnostic capabilities of hs-cTnI, hs-cTnT, including consideration of promising possibilities for their study in biological fluids that can be obtained by non-invasive methods. Also, some possibilities of using hs-cTnI and hs-cTnT as prognostic laboratory biomarkers in healthy people (for example, to assess the risk of developing CVD) and in patients suffering from a number of pathological conditions that cause damage to cardiomyocytes are examined, and the potential mechanisms underlying the increase in hs-cTnI and hs-cTnT are discussed.

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State-of-the-art diagnosis of myocardial infarction

Cited by 32 publications

References 28 publications

RETRACTED: Skullcapflavone I protects cardiomyocytes from hypoxia-caused injury through up-regulation of lincRNA-ROR

RETRACTED: Skullcapflavone I protects cardiomyocytes from hypoxia-caused injury through up-regulation of lincRNA-ROR

lncRNA GAS5 regulates myocardial infarction by targeting the miR‐525‐5p/CALM2 axis

Cardiac Troponins: Contemporary Biological Data and New Methods of Determination

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