Cardiac Troponins Metabolism: From Biochemical Mechanisms to Clinical Practice (Literature Review)

Chaulin, Aleksey M.

doi:10.3390/ijms222010928

Cited by 49 publications

(34 citation statements)

References 112 publications

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“…These are ERKs (extracellular-signal-regulated kinases), JNKs, and p38/SAPKs (stress-activated protein kinases) in mammals [ 18 ]. JNK is activated and transferred to the nucleus, stimulating the transcription factor c-Jun and its phosphorylation, promoting apoptosis, and differentiation [ 19 ]. Tumor necrosis factor-alpha (TNF- α ) is an essential regulator of apoptosis and inflammation.…”

Section: Introductionmentioning

confidence: 99%

Inhibition of TNF-α and JNK Signaling Pathway Can Reduce Paclitaxel-Induced Apoptosis of Mouse Cardiomyocytes

Ren

Huang

et al. 2022

Applied Bionics and Biomechanics

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Paclitaxel (PTX) is a widely used chemotherapeutic drug for treating tumors. However, studies have shown that it can cause cardiac problems such as arrhythmia, myocarditis, chronic cardiomyopathy, and heart failure. Therefore, it is essential to study the mechanism behind the cardiotoxicity of PTX in tumor treatment. In this study, we initially injected PTX into mice to establish a myocardial cell apoptosis model to observe the degree of damage to mouse myocardium caused by PTX. Upon determining the levels of mouse myocardial creatine phosphokinase (CK), myokinase isoenzyme (CK-MB), aspartate transaminase (AST), and lactate dehydrogenase (LDH), we found that all of these levels showed apparent increases in mice treated with PTX. Further analyses of the TNF-α level and the expression of Jun N-terminal kinase (JNK) and Bcl-2 family-related proteins in myocardial tissue were performed. It was found that PTX increased the protein levels of TNF-α, Bax, p-JNK, and JNK in myocardial tissue but decreased the protein level of Bcl-2. After 1 month of PTX treatment in mice, we inhibited the expression of TNF-α and JNK proteins, which reduced the effect of paclitaxel on the apoptosis of mouse cardiomyocytes. The protein levels of Bax, p-JNK, and TNF-α in cardiomyocytes were reduced, while there was a relative increase in the Bcl-2 protein level. The findings suggested that inhibition of the NK signaling pathway and TNF-α can lessen the effect of PTX on mouse cardiomyocytes.

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Section: Introductionmentioning

confidence: 99%

Inhibition of TNF-α and JNK Signaling Pathway Can Reduce Paclitaxel-Induced Apoptosis of Mouse Cardiomyocytes

Ren

Huang

et al. 2022

Applied Bionics and Biomechanics

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“…Cross-reactions of the diagnostic antibodies of troponin immunoassays with skeletal muscle troponin isoforms arising in diseases and injuries of skeletal muscles (myopathy, rhabdomyolysis, etc.) were considered frequent when using "outdated" immunoassays of the first and second generation [114][115][116][117][118][119]. Nevertheless, several cases have been described in which modern test systems, including monoclonal antibodies that are part of modern highly sensitive methods, also reacted to skeletal troponin isoforms, being more typical for troponin T [120,121].…”

Section: Autoantibodiesmentioning

confidence: 99%

Elevation Mechanisms and Diagnostic Consideration of Cardiac Troponins under Conditions Not Associated with Myocardial Infarction. Part 2

Chaulin

2021

Life

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This article proceeds with a discussion of the causes and mechanisms of an elevation in cardiac troponins in pathological conditions not associated with acute myocardial infarction. The second part of the article discusses the causes and mechanisms of cardiac troponins elevation in diabetes mellitus, arterial hypertension, hereditary cardiomyopathies, cardiac arrhythmias (atrial fibrillation, supraventricular tachycardia), acute aortic dissection, and diseases of the central nervous system (strokes, subarachnoidal hemorrhage). The final chapter of this article discusses in detail the false-positive causes and mechanisms of elevated cardiac troponins.

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“…Cardiac troponins (troponin T (cTnT) and troponin I (cTnI)) are the main and most specific biomarkers for the early diagnosis of acute myocardial infarction (AMI) [ 1 - 4 ]. In accordance with the main guidance document (Fourth Universal Definition of Myocardial Infarction), the main criteria for AMI are the following: 1) myocardial damage detected using cTns; 2) symptoms of myocardial ischemia; 3) ischemic changes on an electrocardiogram and in particular the appearance of a pathological Q wave; 4) identification of areas of non-viable myocardium using imaging methods; and 5) detection of a blood clot in the coronary arteries using coronary angiography or autopsy [ 1 ].…”

Section: Introductionmentioning

confidence: 99%

False-Positive Causes in Serum Cardiac Troponin Levels

Chaulin

2022

J Clin Med Res

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Cardiac troponins (cTns) are the most valuable and specific markers of cardiovascular diseases, including acute myocardial infarction. These biomarkers can also be used to assess the degree of myocardial damage in non-cardiac diseases that can negatively affect the cells of cardiac muscle tissue. However, in everyday clinical practice, doctors often encounter with false-positive cases of increased cTns. Falsepositive cases of increased cTns can contribute to incorrect diagnosis and subsequent inadequate treatment, which causes significant harm to the patient. This review discusses some common causes of a falsepositive increase in the level of cTns in the blood serum. Such causes are fibrin clots, heterophilic antibodies, alkaline phosphatase, rheumatoid factor, and cross-reactions of diagnostic (anti-cTn) antibodies with skeletal troponins. Detailed attention is focused on the mechanisms of false-positive increase, and ways to identify and combat these false-positive causes of increased cTns. This has an important practical significance in modern clinical practice.

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Cardiac Troponins Metabolism: From Biochemical Mechanisms to Clinical Practice (Literature Review)

Cited by 49 publications

References 112 publications

Inhibition of TNF-α and JNK Signaling Pathway Can Reduce Paclitaxel-Induced Apoptosis of Mouse Cardiomyocytes

Inhibition of TNF-α and JNK Signaling Pathway Can Reduce Paclitaxel-Induced Apoptosis of Mouse Cardiomyocytes

Elevation Mechanisms and Diagnostic Consideration of Cardiac Troponins under Conditions Not Associated with Myocardial Infarction. Part 2

False-Positive Causes in Serum Cardiac Troponin Levels

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