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- Cardiac troponins are a group of proteins found in cardiac muscle cells (myocardium) that play a crucial role in regulating the contraction of the heart. They are involved in the process of muscle contraction by interacting with the protein complex actin and myosin, which are responsible for the mechanical function of the heart.
There are three main subunits of troponin:
Troponin C (TnC): This subunit binds to calcium ions, which is a key step in the initiation of muscle contraction. When calcium ions bind to troponin C, it triggers a series of events that lead to the exposure of binding sites on actin, allowing myosin to interact with actin and initiate muscle contraction.
Troponin I (TnI): Troponin I inhibits the interaction between actin and myosin when the muscle is at rest. When the muscle needs to contract, the binding of calcium ions to troponin C causes a conformational change in troponin I, releasing its inhibitory effect and allowing muscle contraction to occur.
Troponin T (TnT): Troponin T anchors the troponin complex to the tropomyosin, another protein that plays a role in regulating muscle contraction. This interaction is essential for the proper functioning of the troponin-tropomyosin complex.
Cardiac troponins are of particular clinical importance because they are released into the bloodstream when cardiac muscle cells are damaged or injured. Therefore, measuring the levels of cardiac troponins in the blood is a common diagnostic tool used to assess and diagnose various heart-related conditions, particularly myocardial infarction (heart attack). When heart muscle cells are damaged due to reduced blood flow (ischemia) or other causes, troponins leak into the bloodstream, and their elevated levels indicate potential heart damage.
Due to their high sensitivity and specificity for cardiac muscle injury, cardiac troponin tests have become a critical component of diagnosing and managing heart-related conditions in clinical practice.
"Acute cardiac injury, defined as significant elevation of cardiac troponins, is the most commonly reported cardiac abnormality in COVID-19 patients." (Bansal, 2020).
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"Excessive F ingestion induces Ca2+ metabolic disorder, and an abnormal expression of cardiac troponins are involved in F-induced cardiomyocyte damage." (Wang et al. 2018)
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(SEE: Green Tea)
Ismail HTH - "The Impact of Iodine Exposure in Excess on Hormonal Aspects and Hemato-Biochemical Profile in Rats" Biol Trace Elem Res 200(2):706-719 (2022). doi: 10.1007/s12011-021-02681-7
https://link.springer.com/article/10.10 ... 21-02681-7
"Overall results revealed that excess iodine in both tested groups developed a hyperthyroid condition, hypercortisolism, relative polycythemia, neutropenia, elevation in serum liver and cardiac enzymes activities, hyperprotenemia, hyperglobulinemia, elevation in serum urea, and cardiac troponin I concentrations (p < 0.05)."
Ca2+ = transduced by Gq/11
Frey UH, Lieb W, Erdmann J, Savidou D, Heusch G, Leineweber K, Jakob H, Hense HW, Löwel H, Brockmeyer NH, Schunkert H, Siffert W - "Characterization of the GNAQ promoter and association of increased Gq expression with cardiac hypertrophy in humans" Eur Heart J 29(7):888-97 (2008) doi: 10.1093/eurheartj/ehm618. Epub 2008 Mar 6. PMID: 18326504
SEE ALSO: NF-kappa B. viewtopic.php?f=66&t=1888
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https://www.ncbi.nlm.nih.gov/pmc/articl ... 9753-g004/
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Watanabe N, Yoshimura Noh J, Hattori N, Iwaku K, Suzuki N, Yoshihara A, Ohye H, Suzuki M, Matsumoto M, Endo K, Kunii Y, Takagi G, Sugino K, Ito K - "Cardiac Troponin Is Elevated in Patients with Thyrotoxicosis and Decreases as Thyroid Function Improves and Brain Natriuretic Peptide Levels Decrease" Eur Thyroid J 10(6):468-475 (2021) doi: 10.1159/000510619
"In thyrotoxicosis, the myocardial biomarker hsTnI is elevated in about 20% of patients; hsTnI levels decrease as thyroid function improves and BNP decreases."