Cardiac Troponins

A forum investigating the similarities between COVID-19 and fluoride poisoning, thyroid dysfunction and Gq/11 pathways.
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Cardiac Troponins

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HEART DAMAGE - Cardiac Troponins
© 2020 PFPC
  • 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.
COVID-19

"Acute cardiac injury, defined as significant elevation of cardiac troponins, is the most commonly reported cardiac abnormality in COVID-19 patients." (Bansal, 2020).


Bansal M - "Cardiovascular disease and COVID-19" Diabetes Metab Syndr 14(3):247-250 (2020) doi: 10.1016/j.dsx.2020.03.013. Epub 2020 Mar 25. PMID: 32247212; PMCID: PMC7102662.
https://pubmed.ncbi.nlm.nih.gov/32247212/

Fluoride

"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)


Wang HW, Liu J, Zhao J, Lin L, Zhao WP, Tan PP, Tian WS, Zhou BH - "Ca2+ metabolic disorder and abnormal expression of cardiac troponin involved in fluoride-induced cardiomyocyte damage" Chemosphere 201:564-570 (2018) doi: 10.1016/j.chemosphere.2018.03.053
https://pubmed.ncbi.nlm.nih.gov/29533806/

Oyagbemi AA, Omobowale TO, Ola-Davies OE, Asenuga ER, Ajibade TO, Adejumobi OA, Afolabi JM, Ogunpolu BS, Falayi OO, Saba AB, Adedapo AA, Yakubu MA - "Luteolin-mediated Kim-1/NF-kB/Nrf2 signaling pathways protects sodium fluoride-induced hypertension and cardiovascular complications" Biofactors 44(6):518-531(2018)
doi: 10.1002/biof.1449
https://pubmed.ncbi.nlm.nih.gov/30474894/

Miltonprabu S, Thangapandiyan S - "Epigallocatechin gallate potentially attenuates fluoride-induced oxidative stress mediated cardiotoxicity and dyslipidemia in rats" J Trace Elem Med Biol 29:321-35 (2015) doi: 10.1016/j.jtemb.2014.08.015
https://pubmed.ncbi.nlm.nih.gov/25282272/
(SEE: Green Tea)

Iodine Excess

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)."

Gq/11

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
https://pubmed.ncbi.nlm.nih.gov/18326504/

SEE ALSO: NF-kappa B. viewtopic.php?f=66&t=1888
  • MORE:

    Zheng Z, Peng F, Xu B, Zhao J, Liu H, Peng J, Li Q, Jiang C, Zhou Y, Liu S, Ye C, Zhang P, Xing Y, Guo H, Tang W - "Risk factors of critical & mortal COVID-19 cases: A systematic literature review and meta-analysis." J Infect 23:S0163-4453(20)30234-6 (2020)
    doi: 10.1016/j.jinf.2020.04.021
    https://pubmed.ncbi.nlm.nih.gov/32335169/
Thyroid

Hajje G, Saliba Y, Itani T, Moubarak M, Aftimos G, Farès N - "Hypothyroidism and its rapid correction alter cardiac remodeling" PLoS One 9(10):e109753 (2014) doi: 10.1371/journal.pone.0109753
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4198123/
https://www.ncbi.nlm.nih.gov/pmc/articl ... 9753-g004/

Huang X, Lee KJ, Riedel B, Zhang C, Lemanski LF, Walker JW - "Thyroid hormone regulates slow skeletal troponin I gene inactivation in cardiac troponin I null mouse hearts" J Mol Cell Cardiol 32(12):2221-8 (2000) doi: 10.1006/jmcc.2000.1249. PMID: 11112997
https://pubmed.ncbi.nlm.nih.gov/11112997/

Lee SJ, Kang JG, Ryu OH, et al - "The relationship of thyroid hormone status with myocardial function in stress cardiomyopathy" Eur J Endocrinol. 160(5):799‐806 (2009) doi:10.1530/EJE-08-0808
https://pubmed.ncbi.nlm.nih.gov/19221174/

Machackova J, Barta J, Dhalla NS - "Molecular defects in cardiac myofibrillar proteins due to thyroid hormone imbalance and diabetes" Can J Physiol Pharmacol 83(12):1071‐1091 (2005) doi:10.1139/y05-
https://pubmed.ncbi.nlm.nih.gov/16462907/

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
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8647084/
"In thyrotoxicosis, the myocardial biomarker hsTnI is elevated in about 20% of patients; hsTnI levels decrease as thyroid function improves and BNP decreases."
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