M
Matteo E. Mangoni
Researcher at University of Montpellier
Publications - 95
Citations - 5420
Matteo E. Mangoni is an academic researcher from University of Montpellier. The author has contributed to research in topics: Sinoatrial node & Bradycardia. The author has an hindex of 36, co-authored 87 publications receiving 4774 citations. Previous affiliations of Matteo E. Mangoni include University of Milan & Centre national de la recherche scientifique.
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Journal ArticleDOI
Genesis and Regulation of the Heart Automaticity
Matteo E. Mangoni,Joël Nargeot +1 more
TL;DR: Evidence on the functional role of different families of ion channels in cardiac pacemaking is discussed and recent results obtained on genetically engineered mouse strains displaying dysfunction in heart automaticity are reviewed.
Journal ArticleDOI
Functional role of L-type Cav1.3 Ca2+ channels in cardiac pacemaker activity.
Matteo E. Mangoni,Brigitte Couette,Emmanuel Bourinet,Josef Platzer,Daniel Reimer,Jörg Striessnig,Joël Nargeot +6 more
TL;DR: Genetic evidence is provided linking the activity of genes coding for ionic channels to specific alterations of pacemaker activity of SAN cells to demonstrate that Cav1.3 channels play a major role in the generation of cardiacpacemaker activity by contributing to diastolic depolarization in SAN pacemaker cells.
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Specific pattern of ionic channel gene expression associated with pacemaker activity in the mouse heart
Céline Marionneau,Brigitte Couette,Jie Liu,Huiyu Li,Matteo E. Mangoni,Joël Nargeot,Ming Lei,Denis Escande,Sophie Demolombe +8 more
TL;DR: The present study provides the first genome‐scale regional ionic channel expression profile in the mouse heart by using large‐scale real‐time RT‐PCR and two‐way hierarchical clustering analysis of the 71 genes successfully classified the six pools from the four distinct regions.
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Bradycardia and Slowing of the Atrioventricular Conduction in Mice Lacking CaV3.1/α1G T-Type Calcium Channels
Matteo E. Mangoni,Achraf Traboulsie,Anne-Laure Leoni,Brigitte Couette,Laurine Marger,Khai Le Quang,Elodie Kupfer,Anne Cohen-Solal,José Vilar,Hee-Sup Shin,Denis Escande,Flavien Charpentier,Joël Nargeot,Philippe Lory +13 more
TL;DR: Inactivation of cacna1g significantly slowed the intrinsic in vivo heart rate, prolonged the SAN recovery time, and slowed pacemaker activity of individual SAN cells through a reduction of the slope of the diastolic depolarization.
Journal ArticleDOI
Loss of Ca v 1.3 ( CACNA1D ) function in a human channelopathy with bradycardia and congenital deafness
Shahid Mahmood Baig,Alexandra Koschak,Andreas Lieb,Mathias Gebhart,Claudia Dafinger,Gudrun Nürnberg,Amjad Ali,Ilyas Ahmad,Martina J. Sinnegger-Brauns,Niels Brandt,Niels Brandt,Jutta Engel,Jutta Engel,Matteo E. Mangoni,Muhammad Farooq,Habib U. Khan,Peter Nürnberg,Jörg Striessnig,Hanno J. Bolz +18 more
TL;DR: A human channelopathy with a cardiac and auditory phenotype that closely resembles that of Cacna1d−/− mice is described, which includes deafness and nonconducting calcium channels that had abnormal voltage-dependent gating.