ReviewArchives of biochemistry and biophysics2016
Cardiac troponin structure-function and the influence of hypertrophic cardiomyopathy associated mutations on modulation of contractility.
Review in Archives of biochemistry and biophysics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
33 citing papers in PubMed, 1 synthesis or guideline pooled it, 55 citations in OpenAlex.
- Hypertrophic Cardiomyopathy Mutations of Troponin Reveal Details of Striated Muscle Regulation.Frontiers in physiology · 2022Pooled it
- Human Variant in the Cardiac Troponin I Switch Domain Causes Diastolic Dysfunction in a Novel Mouse Model.Journal of the American Heart Association · 2025Article
- Integrated proteomics identifies troponin I isoform switch as a regulator of a sarcomere-metabolism axis during cardiac regeneration.Cardiovascular research · 2025Article
- Prospects and Challenges of Catechins in Cardiovascular Disease.The AAPS journal · 2025Review
- Hyperactive mTORC1/4EBP1 signaling dysregulates proteostasis and accelerates cardiac aging.GeroScience · 2025Article
- Computational studies on the functional and structural impact of pathogenic mutations in enzymes.Protein science : a publication of the Protein Society · 2025Review
- An FDA-approved drug structurally and phenotypically corrects the K210del mutation in genetic cardiomyopathy models.The Journal of clinical investigation · 2025Article
- Troponin I - a comprehensive review of its function, structure, evolution, and role in muscle diseases.Animal cells and systems · 2025Review
- Data-Driven Insights into the Association Between Oxidative Stress and Calcium-Regulating Proteins in Cardiovascular Disease.Antioxidants (Basel, Switzerland) · 2024Article
- Focus on cardiac troponin complex: From gene expression to cardiomyopathy.Genes & diseases · 2024Review
- Glutamate 139 of tropomyosin is critical for cardiac thin filament blocked-state stabilization.Journal of molecular and cellular cardiology · 2024Article
- Nucleus Mechanosensing in Cardiomyocytes.International journal of molecular sciences · 2023Review
- Diagnostic Role and Methods of Detection of Cardiac Troponins: An Opinion from Historical and Current Points of View.Current cardiology reviews · 2023Review
- Deciphering the Basis of Molecular Biology of Selected Cardiovascular Diseases: A View on Network Medicine.International journal of molecular sciences · 2022Review
- Molecular Diagnosis of Primary Cardiomyopathy in 231 Unrelated Pediatric Cases by Panel-Based Next-Generation Sequencing: A Major Focus on Five Carriers of Biallelic TNNI3 Pathogenic Variants.Molecular diagnosis & therapy · 2022Article
- Dysfunctional sarcomeric relaxation in the heart.Current opinion in physiology · 2022Article
- Significance of Cardiac Troponins as an Identification Tool in COVID-19 Patients Using Biosensors: An Update.Frontiers in molecular biosciences · 2022Review
- Berberine attenuates septic cardiomyopathy by inhibiting TLR4/NF-κB signalling in rats.Pharmaceutical biology · 2021Article
- Cardiac sarcomere mechanics in health and disease.Biophysical reviews · 2021Review
- Fluorescent Immunoassays for Detection and Quantification of Cardiac Troponin I: A Short Review.Molecules (Basel, Switzerland) · 2021Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Cardiac troponin (cTn) acts as a pivotal regulator of muscle contraction and relaxation and is composed of three distinct subunits (cTnC: a highly conserved Ca(2+) binding subunit, cTnI: an actomyosin ATPase inhibitory subunit, and cTnT: a tropomyosin binding subunit). In this mini-review, we briefly summarize the structure-function relationship of cTn and its subunits, its modulation by PKA-mediated phosphorylation of cTnI, and what is known about how these properties are altered by hypertrophic cardiomyopathy (HCM) associated mutations of cTnI. This includes recent work using computational modeling approaches to understand the atomic-based structural level basis of disease-associated mutations. We propose a viewpoint that it is alteration of cTnC-cTnI interaction (rather than the Ca(2+) binding properties of cTn) per se that disrupt the ability of PKA-mediated phosphorylation at cTnI Ser-23/24 to alter contraction and relaxation in at least some HCM-associated mutations. The combination of state of the art biophysical approaches can provide new insight on the structure-function mechanisms of contractile dysfunction resulting cTnI mutations and exciting new avenues for the diagnosis, prevention, and even treatment of heart diseases.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.