Recent Research on Cardiac Troponins
A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Biology".
Deadline for manuscript submissions: closed (28 February 2025) | Viewed by 350
Special Issue Editors
Interests: molecular mechanisms of cardiovascular disease; lipid; troponins
Special Issues, Collections and Topics in MDPI journals
Special Issue Information
Dear Colleagues,
The cardiac troponin complex (cTn) is a regulatory component of sarcomere, consisting of three subunits: cardiac troponin C (cTnC), which confers Ca2+ sensitivity to muscle; cTnI, which inhibits the interaction of myosin cross-bridges with thin filaments during diastole; and cTnT, which has multiple roles in sarcomere, such as promoting the link between the cTnI-cTnC complex and tropomyosin within thin filaments and influencing the Ca2+ sensitivity of cTn and forcing development during contraction. Conditions that interfere with interactions within cTn and/or other thin filament proteins can be key factors in the regulation of cardiac contractions. These conditions include alterations in myofilament Ca2+ sensitivity, direct changes in cTn function, and/or triggering downstream events that lead to adverse cardiac remodeling and impairment of heart function.
Moreover, circulating cTnT and cTnI increase following cardiac tissue necrosis, and they are consolidated biomarkers of acute myocardial infarction. However, the use of high-sensitivity (hs) immunoassay tests for cTnT and cTnI has made it possible to identify a multitude of other clinical conditions associated with increased circulating levels of cTns. cTns can also be measured in the peripheral circulation of healthy subjects or athletes, suggesting that different mechanisms are involved in the release of cTns in the blood independently of cardiac cell necrosis.
This Special Issue aims to evaluate the mechanisms of cTns regulation that can adversely affect the delicate balance among the components of the complex, thereby promoting contractile dysfunction, together with the molecular/cellular processes involved in cTns release in blood and the exploitation of cTnI and cTnT as biomarkers of cardiac adverse events.
Dr. Chiara Caselli
Dr. Rosetta Ragusa
Guest Editors
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Keywords
- cardiac troponin
- gene mutations
- post-translational modifications
- therapy
- high-sensitivity (hs) immunoassays
- mechanisms of release
- biomarkers
- cardiovascular disease
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