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Calmodulin-dependent Signaling01:16

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Calmodulin (CaM) is a calcium-binding protein in eukaryotes that controls various calcium-regulated cellular processes. It has four calcium-binding sites that bind calcium to form the calcium-calmodulin ( Ca2+-CaM) complex. GPCR stimulation increases the calcium levels in the cells that bind to CaM and induces a conformational change.
The Ca2+-CaM complex does not have enzymatic activity by itself. Instead, the complex binds downstream target proteins, including membrane proteins or enzymes,...
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Rheumatic Heart Disease II: Clinical Manifestations and Diagnostic Studies01:22

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The key clinical manifestations of Rheumatic heart disease (RHD) include several distinct cardiac symptoms.Carditis, a hallmark of acute rheumatic fever, involves inflammation of the heart's endocardium, myocardium, and pericardium. Chronic RHD often results from recurrent episodes of carditis. Its symptoms include the following:Murmurs are caused by valvular damage, especially to the mitral and aortic valves. Mitral stenosis or regurgitation is common, with characteristic heart murmurs...
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Rheumatic Heart Disease III: Medical Management01:21

Rheumatic Heart Disease III: Medical Management

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Rheumatic heart disease (RHD) management can be divided into two main strategies: prevention and long-term management.Primary PreventionPrimary prevention focuses on timely diagnosis and management of group A streptococcal pharyngitis to prevent acute rheumatic fever. The most widely used antibiotic for treating this condition is intramuscular benzathine penicillin G.Acute Rheumatic Fever TreatmentThe primary treatment goal for a patient diagnosed with acute rheumatic fever is to suppress the...
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Rheumatic Heart Disease I: Introduction01:23

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Rheumatic heart disease or RHD is a chronic condition that results from rheumatic fever, causing permanent damage to the heart valves.Etiology and Risk FactorsIt primarily arises from rheumatic fever, an inflammatory disease that can develop after untreated or inadequately treated group A streptococcal (GAS) pharyngitis. Streptococcus spreads through direct contact with oral or respiratory secretions. While the bacteria are the causative agents, factors like malnutrition, overcrowding, poor...
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cAMP-dependent Protein Kinase Pathways01:25

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Cyclic Adenosine Monophosphate (cAMP) is an essential second messenger that activates protein kinase A (PKA) and regulates various biological processes. A single epinephrine molecule binds to GPCR and activates several heterotrimeric G proteins, each stimulating multiple adenylyl cyclase, amplifying the signal, and synthesizing large numbers of cAMP molecules. Small changes in cAMP concentration affect PKA activity. The binding of four cAMP molecules induces a conformational change in PKA,...
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Clinical manifestationsPeripheral Arterial Disease (PAD) manifests through a range of symptoms, from the characteristic intermittent claudication to atypical presentations and severe complications in advanced stages. Intermittent claudication, a hallmark symptom of PAD, presents as exercise-induced muscle pain that typically resolves within minutes of rest. This pain is reproducible and stems from inadequate blood flow, leading to the accumulation of lactic acid produced during anaerobic...
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Updated: Sep 9, 2025

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Las calmodulinopatías: la necesidad de un registro

Peter J Schwartz1, Lia Crotti2

  • 1Istituto Auxologico Italiano IRCCS, Center for Cardiac Arrhythmias of Genetic Origin and Laboratory of Cardiovascular Genetics, Milano, Italy.

JACC. Clinical electrophysiology
|September 3, 2025
PubMed
Resumen
Este resumen es generado por máquina.

Las calmodulinopatías son trastornos genéticos raros relacionados con la muerte súbita cardíaca. La inscripción de pacientes en el Registro Internacional de Calmodulinopatía es crucial para comprender los mecanismos de la enfermedad y mejorar el manejo del paciente.

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Área de la Ciencia:

  • Cardiología
  • La genética
  • Biología molecular

Sus antecedentes:

  • Las calmodulinopatías son trastornos genéticos raros con un alto riesgo de muerte súbita cardíaca.
  • Las variantes causantes de la enfermedad en los genes CALM conducen a síndrome de QT largo grave, taquicardia ventricular polimórfica catecolaminérgica y fibrilación ventricular idiopática.
  • El conocimiento actual se basa en datos limitados del Registro Internacional de Calmodulinopatía (ICamR), lo que dificulta el progreso.

Objetivo del estudio:

  • Para hacer frente a la lenta acumulación de pacientes en el ICamR.
  • Solicitar la participación global de los médicos en la inscripción de pacientes, incluidos los casos aislados.
  • Recopilar datos suficientes para una correlación genotipo-fenotipo completa y mejorar la estratificación del riesgo.

Principales métodos:

  • Un llamado a la acción para que los médicos de todo el mundo contribuyan con los datos de los pacientes al ICamR.
  • Aprovechar los conocimientos existentes de iniciativas anteriores para el síndrome del intervalo QT largo.
  • Establecimiento de un registro colaborativo para los trastornos genéticos cardíacos raros.

Principales resultados:

  • La acumulación actual de pacientes en ICamR es insuficiente para una investigación científica sólida.
  • Existe una brecha significativa en la comprensión del espectro clínico completo y las correlaciones genotipo- fenotipo.
  • La mejora de la recopilación de datos es esencial para avanzar en el tratamiento de las calmodulinopatías.

Conclusiones:

  • Se necesita con urgencia una mayor inscripción de pacientes en el ICamR.
  • Los datos completos son vitales para definir las manifestaciones de la enfermedad y orientar las estrategias terapéuticas.
  • La colaboración global es clave para avanzar en la investigación de las canalopatías cardíacas raras como las calmodulinopatías.