Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Mavacamten rescues increased myofilament calcium sensitivity and dysregulation of Ca2+ flux caused by thin filament hypertrophic cardiomyopathy mutations.

American journal of physiology. Heart and circulatory physiology - 1 Mar 2020

Sparrow Alexander J, Watkins Hugh, Daniels Matthew J, Redwood Charles, Robinson Paul

Abstract excerpt

Thin filament hypertrophic cardiomyopathy (HCM) mutations increase myofilament Ca2+ sensitivity and alter Ca2+ handling and buffering. The myosin inhibitor mavacamten reverses the increased contractility caused by HCM thick filament mutations, and we here test its effect on HCM thin filament mutations where the mode of action is not known. Mavacamten (250 nM) partially reversed the increased Ca2+ sensitivity...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Benzylamines
Share to Cardiomyopathy, Hypertrophic

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Myocytes, Cardiac

Share to Sarcomeres

Share to Troponin I

Share to Troponin T

Share to Uracil

Source

Open in PubMed Open full text

Identifiers

PMID: 32083971
DOI: 10.1152/ajpheart.00023.2020
PMCID: PMC7099453

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 1 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Mavacamten rescues increased myofilament calcium sensitivity and dysregulation of Ca2+ flux caused by thin filament hypertrophic cardiomyopathy mutations.PMID 32083971Read ↗

Mutations in Troponin that cause HCM, DCM AND RCM: what can we learn about thin filament function?Semantic proximity Read ↗

Mavacamten decreases maximal force and Ca2+ sensitivity in the N47K-myosin regulatory light chain mouse model of hypertrophic cardiomyopathy.Semantic proximity Read ↗

Thin filament cardiomyopathies: A review of genetics, disease mechanisms, and emerging therapeuticsSemantic proximity Read ↗

Mavacamten shows broad benefit in human and mouse models of MYBPC3-related hypertrophic cardiomyopathy.Semantic proximity Read ↗

Cardiac Troponin and Tropomyosin: Structural and Cellular Perspectives to Unveil the Hypertrophic Cardiomyopathy PhenotypeSemantic proximity Read ↗

Enhanced myofilament calcium sensitivity aggravates abnormal calcium handling and diastolic dysfunction in patient-specific induced pluripotent stem cell-derived cardiomyocytes with MYH7 mutation.Semantic proximity Read ↗

Dilated and hypertrophic cardiomyopathy mutations in troponin and alpha-tropomyosin have opposing effects on the calcium affinity of cardiac thin filaments.Semantic proximity Read ↗

Impaired calcium handling and mitochondrial metabolic dysfunction as early markers of hypertrophic cardiomyopathySemantic proximity Read ↗

Hypertrophic cardiomyopathy: an up-to-date snapshot of the clinical drug development pipeline.Semantic proximity Read ↗

Mechanism based therapies enable personalised treatment of hypertrophic cardiomyopathy.Semantic proximity Read ↗

Long-term mavacamten exposure reduces force and sarcomere density in a hiPSC model of hypertrophic cardiomyopathySemantic proximity Read ↗

Aficamten is a small-molecule cardiac myosin inhibitor designed to treat hypertrophic cardiomyopathy.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.