更新于：2024-11-01

肌钙蛋白C

更新于：2024-11-01

基本信息

别名-

简介-

关联

项与肌钙蛋白C 相关的药物

TnCL-48Q

靶点

肌钙蛋白C

作用机制

肌钙蛋白C调节剂

在研机构

The Ohio State University Wexner Medical Center

原研机构

The Ohio State University Wexner Medical Center

在研适应症

心脏病

非在研适应症-

最高研发阶段临床前

首次获批国家/地区-

首次获批日期1800-01-20

100 项与肌钙蛋白C 相关的临床结果

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100 项与肌钙蛋白C 相关的转化医学

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0 项与肌钙蛋白C 相关的专利（医药）

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1,840

项与肌钙蛋白C 相关的文献（医药）

2024-11-26·Clinical Chemistry and Laboratory Medicine (CCLM)

Analytical validation of the Mindray CL1200i analyzer high sensitivity cardiac troponin I assay: MERITnI study

Article

作者: Schulz, Karen ; Fabre-Estremera, Blanca ; Apple, Fred S. ; Sexter, Anne ; Ladd, Alanna

AbstractObjectivesThis study performed an analytical validation study of the Mindray high-sensitivity cardiac troponin I (hs-cTnI) assay addressing limit of blank (LoB), limit of detection (LoD), precision, linearity, analytical specificity and sex-specific 99th percentile upper reference limits.MethodsLoB, LoD, precision, linearity and analytical specificity were studied according to Clinical and Laboratory Standards Institute. We used one reagent lot and one CL1200i analyzer. Skeletal troponin I and T, cardiac troponin T, troponin C, actin, tropomyosin, myosin light chain, myoglobin and creatine kinase (CK-MB) were studied for cross-reactivity. Interference with biotin was examined. Lithium heparin samples (one freeze thaw cycle) from healthy males and females were measured to determine the 99th percentiles by using the non-parametric method. Analyses were performed before and after excluding subjects with clinical conditions and/or increased surrogate biomarkers.ResultsThe Mindray hs-cTnI assay met criteria to be considered as a hs-cTn assay. LoB and LoD was <0.1 ng/L and 0.1 ng/L, respectively. Repeatability had a coefficient of variation 1.2–3.8 %, and within-laboratory imprecision 1.7–5.0 %. The measuring interval ranged from 1.1 to 28,180 ng/L. The analytical specificity was clinically acceptable for the interferents studied. After exclusions, the 99th percentile URLs obtained were 10 ng/L overall, 5 ng/L for females and 12 ng/L for males.ConclusionsAnalytical observations of the Mindray hs-cTnI assay demonstrated excellent LoB, LoD, precision, linearity and analytical specificity, that were in alignment with the manufacturer’s claims and regulatory guidelines for hs-cTnI. The assay is suitable for clinical investigation for patient-oriented studies.

2024-11-01·Gene

Troponin C gene mutations on cardiac muscle cell and skeletal Regulation: A comprehensive review

Review

作者: Onifade, Isreal Ayobami ; Abok, Jeremiah I ; Adeoye, Adekunle Fatai ; Aborode, Abdullahi Tunde ; Idris, Ibrahim ; Aluko, Babatunde Akinola ; Olamilekan Adesola, Ridwan ; Scott, Godfred Yawson ; Chakoma, Mugove ; Adio, Waheed Sakariyau ; Oluwaseun, Adereti Ayomide

BACKGROUNDThe troponin complex plays a crucial role in regulating skeletal and cardiac contraction. Congenital myopathies can occur due to several mutations in genes that encode skeletal troponin. Moreover, there is limited information regarding the composition of skeletal troponin. This review specifically examines a comprehensive review of the TNNC gene mutations on cardiac and skeletal regulations.MAIN BODYTroponin C (TNNC) has been linked to a newly discovered inherited muscle disorder. Genetic variations in genes that encode skeletal troponin can impair the function of sarcomeres. Various treatment approaches have been employed to mitigate the impact of variations, including the use of troponin activators, the injection of wild-type protein via AAV gene therapy, and myosin modification to enhance muscle contraction. The processes responsible for the pathophysiological implications of the variations in genes that encode skeletal troponin are not fully understood.CONCLUSIONThis comprehensive review will contribute to the understanding of the relationship between human cardiomyopathy and TNNC mutations and will guide the development of therapy approaches.

2024-09-15·Biology Open

A larval zebrafish model of cardiac physiological recovery following cardiac arrest and myocardial hypoxic damage

Article

作者: Hansson, Kenny ; Wang, Qing-Dong ; Patel, Vishal ; Jagadeeswaran, Pudur ; Iyer, Neha ; Trivedi, Hersh ; Raman, Revathi ; Rydén-Markinhutha, Katarina ; Burggren, Warren ; Jennbacken, Karin ; Bautista, Naim M. ; Fritsche Danielson, Regina ; Dubansky, Ben ; Williams, Steven ; Vazquez Roman, Karem ; Abramova, Regina ; Gupta, Avi

ABSTRACTContemporary cardiac injury models in zebrafish larvae include cryoinjury, laser ablation, pharmacological treatment and cardiac dysfunction mutations. Although effective in damaging cardiomyocytes, these models lack the important element of myocardial hypoxia, which induces critical molecular cascades within cardiac muscle. We have developed a novel, tractable, high throughput in vivo model of hypoxia-induced cardiac damage that can subsequently be used in screening cardioactive drugs and testing recovery therapies. Our potentially more realistic model for studying cardiac arrest and recovery involves larval zebrafish (Danio rerio) acutely exposed to severe hypoxia (PO2=5-7 mmHg). Such exposure induces loss of mobility quickly followed by cardiac arrest occurring within 120 min in 5 days post fertilization (dpf) and within 40 min at 10 dpf. Approximately 90% of 5 dpf larvae survive acute hypoxic exposure, but survival fell to 30% by 10 dpf. Upon return to air-saturated water, only a subset of larvae resumed heartbeat, occurring within 4 min (5 dpf) and 6-8 min (8-10 dpf). Heart rate, stroke volume and cardiac output in control larvae before hypoxic exposure were 188±5 bpm, 0.20±0.001 nL and 35.5±2.2 nL/min (n=35), respectively. After briefly falling to zero upon severe hypoxic exposure, heart rate returned to control values by 24 h of recovery. However, reflecting the severe cardiac damage induced by the hypoxic episode, stroke volume and cardiac output remained depressed by ∼50% from control values at 24 h of recovery, and full restoration of cardiac function ultimately required 72 h post-cardiac arrest. Immunohistological staining showed co-localization of Troponin C (identifying cardiomyocytes) and Capase-3 (identifying cellular apoptosis). As an alternative to models employing mechanical or pharmacological damage to the developing myocardium, the highly reproducible cardiac effects of acute hypoxia-induced cardiac arrest in the larval zebrafish represent an alternative, potentially more realistic model that mimics the cellular and molecular consequences of an infarction for studying cardiac tissue hypoxia injury and recovery of function.