The Experts below are selected from a list of 48 Experts worldwide ranked by ideXlab platform
Matteo E Mangoni - One of the best experts on this subject based on the ideXlab platform.
-
Correction to: Channelopathies of voltage-gated L-type Cav1.3/α_1D and T-type Cav3.1/α_1G Ca^2+ channels in dysfunction of Heart Automaticity
Pflügers Archiv - European Journal of Physiology, 2020Co-Authors: Angelo G Torrente, Pietro Mesirca, Isabelle Bidaud, Matteo E MangoniAbstract:The above article was published online with an error in Fig. 1b. There is a doubled action potential at the far right of the left panel of the figure.
-
Correction to: Channelopathies of voltage-gated L-type Cav1.3/α1D and T-type Cav3.1/α1G Ca2+ channels in dysfunction of Heart Automaticity.
Pflugers Archiv : European journal of physiology, 2020Co-Authors: Angelo G Torrente, Pietro Mesirca, Isabelle Bidaud, Matteo E MangoniAbstract:The above article was published online with an error in Fig. 1b. There is a doubled action potential at the far right of the left panel of the figure.
-
correction to channelopathies of voltage gated l type cav1 3 α1d and t type cav3 1 α1g ca2 channels in dysfunction of Heart Automaticity
Pflügers Archiv: European Journal of Physiology, 2020Co-Authors: Angelo G Torrente, Pietro Mesirca, Isabelle Bidaud, Matteo E MangoniAbstract:The above article was published online with an error in Fig. 1b. There is a doubled action potential at the far right of the left panel of the figure.
-
Channelopathies of voltage-gated L-type Cav1.3/α_1D and T-type Cav3.1/α_1G Ca^2+ channels in dysfunction of Heart Automaticity
Pflügers Archiv - European Journal of Physiology, 2020Co-Authors: Angelo G Torrente, Pietro Mesirca, Isabelle Bidaud, Matteo E MangoniAbstract:The Heart Automaticity is a fundamental physiological function in vertebrates. The cardiac impulse is generated in the sinus node by a specialized population of spontaneously active myocytes known as “pacemaker cells.” Failure in generating or conducting spontaneous activity induces dysfunction in cardiac Automaticity. Several families of ion channels are involved in the generation and regulation of the Heart Automaticity. Among those, voltage-gated L-type Cav1.3 (α1D) and T-type Cav3.1 (α1G) Ca^2+ channels play important roles in the spontaneous activity of pacemaker cells. Ca^2+ channel channelopathies specifically affecting cardiac Automaticity are considered rare. Recent research on familial disease has identified mutations in the Cav1.3-encoding CACNA1D gene that underlie congenital sinus node dysfunction and deafness (OMIM # 614896). In addition, both Cav1.3 and Cav3.1 channels have been identified as pathophysiological targets of sinus node dysfunction and Heart block, caused by congenital autoimmune disease of the cardiac conduction system. The discovery of channelopathies linked to Cav1.3 and Cav3.1 channels underscores the importance of Ca^2+ channels in the generation and regulation of Heart’s Automaticity.
-
Channelopathies of voltage-gated L-type Cav1.3/α1D and T-type Cav3.1/α1G Ca2+ channels in dysfunction of Heart Automaticity.
Pflugers Archiv : European journal of physiology, 2020Co-Authors: Angelo G Torrente, Pietro Mesirca, Isabelle Bidaud, Matteo E MangoniAbstract:The Heart Automaticity is a fundamental physiological function in vertebrates. The cardiac impulse is generated in the sinus node by a specialized population of spontaneously active myocytes known as "pacemaker cells." Failure in generating or conducting spontaneous activity induces dysfunction in cardiac Automaticity. Several families of ion channels are involved in the generation and regulation of the Heart Automaticity. Among those, voltage-gated L-type Cav1.3 (α1D) and T-type Cav3.1 (α1G) Ca2+ channels play important roles in the spontaneous activity of pacemaker cells. Ca2+ channel channelopathies specifically affecting cardiac Automaticity are considered rare. Recent research on familial disease has identified mutations in the Cav1.3-encoding CACNA1D gene that underlie congenital sinus node dysfunction and deafness (OMIM # 614896). In addition, both Cav1.3 and Cav3.1 channels have been identified as pathophysiological targets of sinus node dysfunction and Heart block, caused by congenital autoimmune disease of the cardiac conduction system. The discovery of channelopathies linked to Cav1.3 and Cav3.1 channels underscores the importance of Ca2+ channels in the generation and regulation of Heart's Automaticity.
Angelo G Torrente - One of the best experts on this subject based on the ideXlab platform.
-
Correction to: Channelopathies of voltage-gated L-type Cav1.3/α_1D and T-type Cav3.1/α_1G Ca^2+ channels in dysfunction of Heart Automaticity
Pflügers Archiv - European Journal of Physiology, 2020Co-Authors: Angelo G Torrente, Pietro Mesirca, Isabelle Bidaud, Matteo E MangoniAbstract:The above article was published online with an error in Fig. 1b. There is a doubled action potential at the far right of the left panel of the figure.
-
Correction to: Channelopathies of voltage-gated L-type Cav1.3/α1D and T-type Cav3.1/α1G Ca2+ channels in dysfunction of Heart Automaticity.
Pflugers Archiv : European journal of physiology, 2020Co-Authors: Angelo G Torrente, Pietro Mesirca, Isabelle Bidaud, Matteo E MangoniAbstract:The above article was published online with an error in Fig. 1b. There is a doubled action potential at the far right of the left panel of the figure.
-
correction to channelopathies of voltage gated l type cav1 3 α1d and t type cav3 1 α1g ca2 channels in dysfunction of Heart Automaticity
Pflügers Archiv: European Journal of Physiology, 2020Co-Authors: Angelo G Torrente, Pietro Mesirca, Isabelle Bidaud, Matteo E MangoniAbstract:The above article was published online with an error in Fig. 1b. There is a doubled action potential at the far right of the left panel of the figure.
-
Channelopathies of voltage-gated L-type Cav1.3/α_1D and T-type Cav3.1/α_1G Ca^2+ channels in dysfunction of Heart Automaticity
Pflügers Archiv - European Journal of Physiology, 2020Co-Authors: Angelo G Torrente, Pietro Mesirca, Isabelle Bidaud, Matteo E MangoniAbstract:The Heart Automaticity is a fundamental physiological function in vertebrates. The cardiac impulse is generated in the sinus node by a specialized population of spontaneously active myocytes known as “pacemaker cells.” Failure in generating or conducting spontaneous activity induces dysfunction in cardiac Automaticity. Several families of ion channels are involved in the generation and regulation of the Heart Automaticity. Among those, voltage-gated L-type Cav1.3 (α1D) and T-type Cav3.1 (α1G) Ca^2+ channels play important roles in the spontaneous activity of pacemaker cells. Ca^2+ channel channelopathies specifically affecting cardiac Automaticity are considered rare. Recent research on familial disease has identified mutations in the Cav1.3-encoding CACNA1D gene that underlie congenital sinus node dysfunction and deafness (OMIM # 614896). In addition, both Cav1.3 and Cav3.1 channels have been identified as pathophysiological targets of sinus node dysfunction and Heart block, caused by congenital autoimmune disease of the cardiac conduction system. The discovery of channelopathies linked to Cav1.3 and Cav3.1 channels underscores the importance of Ca^2+ channels in the generation and regulation of Heart’s Automaticity.
-
Channelopathies of voltage-gated L-type Cav1.3/α1D and T-type Cav3.1/α1G Ca2+ channels in dysfunction of Heart Automaticity.
Pflugers Archiv : European journal of physiology, 2020Co-Authors: Angelo G Torrente, Pietro Mesirca, Isabelle Bidaud, Matteo E MangoniAbstract:The Heart Automaticity is a fundamental physiological function in vertebrates. The cardiac impulse is generated in the sinus node by a specialized population of spontaneously active myocytes known as "pacemaker cells." Failure in generating or conducting spontaneous activity induces dysfunction in cardiac Automaticity. Several families of ion channels are involved in the generation and regulation of the Heart Automaticity. Among those, voltage-gated L-type Cav1.3 (α1D) and T-type Cav3.1 (α1G) Ca2+ channels play important roles in the spontaneous activity of pacemaker cells. Ca2+ channel channelopathies specifically affecting cardiac Automaticity are considered rare. Recent research on familial disease has identified mutations in the Cav1.3-encoding CACNA1D gene that underlie congenital sinus node dysfunction and deafness (OMIM # 614896). In addition, both Cav1.3 and Cav3.1 channels have been identified as pathophysiological targets of sinus node dysfunction and Heart block, caused by congenital autoimmune disease of the cardiac conduction system. The discovery of channelopathies linked to Cav1.3 and Cav3.1 channels underscores the importance of Ca2+ channels in the generation and regulation of Heart's Automaticity.
Pietro Mesirca - One of the best experts on this subject based on the ideXlab platform.
-
Correction to: Channelopathies of voltage-gated L-type Cav1.3/α_1D and T-type Cav3.1/α_1G Ca^2+ channels in dysfunction of Heart Automaticity
Pflügers Archiv - European Journal of Physiology, 2020Co-Authors: Angelo G Torrente, Pietro Mesirca, Isabelle Bidaud, Matteo E MangoniAbstract:The above article was published online with an error in Fig. 1b. There is a doubled action potential at the far right of the left panel of the figure.
-
Correction to: Channelopathies of voltage-gated L-type Cav1.3/α1D and T-type Cav3.1/α1G Ca2+ channels in dysfunction of Heart Automaticity.
Pflugers Archiv : European journal of physiology, 2020Co-Authors: Angelo G Torrente, Pietro Mesirca, Isabelle Bidaud, Matteo E MangoniAbstract:The above article was published online with an error in Fig. 1b. There is a doubled action potential at the far right of the left panel of the figure.
-
correction to channelopathies of voltage gated l type cav1 3 α1d and t type cav3 1 α1g ca2 channels in dysfunction of Heart Automaticity
Pflügers Archiv: European Journal of Physiology, 2020Co-Authors: Angelo G Torrente, Pietro Mesirca, Isabelle Bidaud, Matteo E MangoniAbstract:The above article was published online with an error in Fig. 1b. There is a doubled action potential at the far right of the left panel of the figure.
-
Channelopathies of voltage-gated L-type Cav1.3/α_1D and T-type Cav3.1/α_1G Ca^2+ channels in dysfunction of Heart Automaticity
Pflügers Archiv - European Journal of Physiology, 2020Co-Authors: Angelo G Torrente, Pietro Mesirca, Isabelle Bidaud, Matteo E MangoniAbstract:The Heart Automaticity is a fundamental physiological function in vertebrates. The cardiac impulse is generated in the sinus node by a specialized population of spontaneously active myocytes known as “pacemaker cells.” Failure in generating or conducting spontaneous activity induces dysfunction in cardiac Automaticity. Several families of ion channels are involved in the generation and regulation of the Heart Automaticity. Among those, voltage-gated L-type Cav1.3 (α1D) and T-type Cav3.1 (α1G) Ca^2+ channels play important roles in the spontaneous activity of pacemaker cells. Ca^2+ channel channelopathies specifically affecting cardiac Automaticity are considered rare. Recent research on familial disease has identified mutations in the Cav1.3-encoding CACNA1D gene that underlie congenital sinus node dysfunction and deafness (OMIM # 614896). In addition, both Cav1.3 and Cav3.1 channels have been identified as pathophysiological targets of sinus node dysfunction and Heart block, caused by congenital autoimmune disease of the cardiac conduction system. The discovery of channelopathies linked to Cav1.3 and Cav3.1 channels underscores the importance of Ca^2+ channels in the generation and regulation of Heart’s Automaticity.
-
Channelopathies of voltage-gated L-type Cav1.3/α1D and T-type Cav3.1/α1G Ca2+ channels in dysfunction of Heart Automaticity.
Pflugers Archiv : European journal of physiology, 2020Co-Authors: Angelo G Torrente, Pietro Mesirca, Isabelle Bidaud, Matteo E MangoniAbstract:The Heart Automaticity is a fundamental physiological function in vertebrates. The cardiac impulse is generated in the sinus node by a specialized population of spontaneously active myocytes known as "pacemaker cells." Failure in generating or conducting spontaneous activity induces dysfunction in cardiac Automaticity. Several families of ion channels are involved in the generation and regulation of the Heart Automaticity. Among those, voltage-gated L-type Cav1.3 (α1D) and T-type Cav3.1 (α1G) Ca2+ channels play important roles in the spontaneous activity of pacemaker cells. Ca2+ channel channelopathies specifically affecting cardiac Automaticity are considered rare. Recent research on familial disease has identified mutations in the Cav1.3-encoding CACNA1D gene that underlie congenital sinus node dysfunction and deafness (OMIM # 614896). In addition, both Cav1.3 and Cav3.1 channels have been identified as pathophysiological targets of sinus node dysfunction and Heart block, caused by congenital autoimmune disease of the cardiac conduction system. The discovery of channelopathies linked to Cav1.3 and Cav3.1 channels underscores the importance of Ca2+ channels in the generation and regulation of Heart's Automaticity.
Isabelle Bidaud - One of the best experts on this subject based on the ideXlab platform.
-
Correction to: Channelopathies of voltage-gated L-type Cav1.3/α_1D and T-type Cav3.1/α_1G Ca^2+ channels in dysfunction of Heart Automaticity
Pflügers Archiv - European Journal of Physiology, 2020Co-Authors: Angelo G Torrente, Pietro Mesirca, Isabelle Bidaud, Matteo E MangoniAbstract:The above article was published online with an error in Fig. 1b. There is a doubled action potential at the far right of the left panel of the figure.
-
Correction to: Channelopathies of voltage-gated L-type Cav1.3/α1D and T-type Cav3.1/α1G Ca2+ channels in dysfunction of Heart Automaticity.
Pflugers Archiv : European journal of physiology, 2020Co-Authors: Angelo G Torrente, Pietro Mesirca, Isabelle Bidaud, Matteo E MangoniAbstract:The above article was published online with an error in Fig. 1b. There is a doubled action potential at the far right of the left panel of the figure.
-
correction to channelopathies of voltage gated l type cav1 3 α1d and t type cav3 1 α1g ca2 channels in dysfunction of Heart Automaticity
Pflügers Archiv: European Journal of Physiology, 2020Co-Authors: Angelo G Torrente, Pietro Mesirca, Isabelle Bidaud, Matteo E MangoniAbstract:The above article was published online with an error in Fig. 1b. There is a doubled action potential at the far right of the left panel of the figure.
-
Channelopathies of voltage-gated L-type Cav1.3/α_1D and T-type Cav3.1/α_1G Ca^2+ channels in dysfunction of Heart Automaticity
Pflügers Archiv - European Journal of Physiology, 2020Co-Authors: Angelo G Torrente, Pietro Mesirca, Isabelle Bidaud, Matteo E MangoniAbstract:The Heart Automaticity is a fundamental physiological function in vertebrates. The cardiac impulse is generated in the sinus node by a specialized population of spontaneously active myocytes known as “pacemaker cells.” Failure in generating or conducting spontaneous activity induces dysfunction in cardiac Automaticity. Several families of ion channels are involved in the generation and regulation of the Heart Automaticity. Among those, voltage-gated L-type Cav1.3 (α1D) and T-type Cav3.1 (α1G) Ca^2+ channels play important roles in the spontaneous activity of pacemaker cells. Ca^2+ channel channelopathies specifically affecting cardiac Automaticity are considered rare. Recent research on familial disease has identified mutations in the Cav1.3-encoding CACNA1D gene that underlie congenital sinus node dysfunction and deafness (OMIM # 614896). In addition, both Cav1.3 and Cav3.1 channels have been identified as pathophysiological targets of sinus node dysfunction and Heart block, caused by congenital autoimmune disease of the cardiac conduction system. The discovery of channelopathies linked to Cav1.3 and Cav3.1 channels underscores the importance of Ca^2+ channels in the generation and regulation of Heart’s Automaticity.
-
Channelopathies of voltage-gated L-type Cav1.3/α1D and T-type Cav3.1/α1G Ca2+ channels in dysfunction of Heart Automaticity.
Pflugers Archiv : European journal of physiology, 2020Co-Authors: Angelo G Torrente, Pietro Mesirca, Isabelle Bidaud, Matteo E MangoniAbstract:The Heart Automaticity is a fundamental physiological function in vertebrates. The cardiac impulse is generated in the sinus node by a specialized population of spontaneously active myocytes known as "pacemaker cells." Failure in generating or conducting spontaneous activity induces dysfunction in cardiac Automaticity. Several families of ion channels are involved in the generation and regulation of the Heart Automaticity. Among those, voltage-gated L-type Cav1.3 (α1D) and T-type Cav3.1 (α1G) Ca2+ channels play important roles in the spontaneous activity of pacemaker cells. Ca2+ channel channelopathies specifically affecting cardiac Automaticity are considered rare. Recent research on familial disease has identified mutations in the Cav1.3-encoding CACNA1D gene that underlie congenital sinus node dysfunction and deafness (OMIM # 614896). In addition, both Cav1.3 and Cav3.1 channels have been identified as pathophysiological targets of sinus node dysfunction and Heart block, caused by congenital autoimmune disease of the cardiac conduction system. The discovery of channelopathies linked to Cav1.3 and Cav3.1 channels underscores the importance of Ca2+ channels in the generation and regulation of Heart's Automaticity.
Joel Nargeot - One of the best experts on this subject based on the ideXlab platform.
-
Heart Automaticity in mice lacking l type cav1 3 and t type cav3 1 ca2 channels insights into the cardiac pacemaker mechanism
Archives of Cardiovascular Diseases Supplements, 2018Co-Authors: M Baudot, Joel Nargeot, Angelo G Torrente, Pietro Mesirca, Isabelle Bidaud, L Fossier, L Talssi, Heesup Shin, Joerg Striessnig, S BarrerelemaireAbstract:Introduction Sino-atrial node (SAN) pacemaker activity is generated by ion channels of the plasma membrane, such as hyperpolarization-activated “funny” f-(HCN), Ca2+ channels and ryanodine receptor (RyR) – dependent Ca2+ release from the sarcoplasmic reticulum (SR). It is currently disputed whether Ca2+ release from RyRs could sustain viable pacemaker activity provided preserved SR Ca2+ content. While working myocytes express L-type Cav1.2 channels to maintain SR Ca2+ content, SAN cells express also L-type Cav1.3 and T-type Cav3.1 channels to generate pacemaking. Objectives We used mutant mice carrying concomitant ablation of Cav1.3 and Cav3.1 (Cav1.3−/−/Cav3.1−/−) to study the importance of these channels in Automaticity. We also investigated the role of f-HCN channels and RyR-dependent Ca2+ release in residual pacemaker activity of mutant mice. Methods We employed in vivo telemetric recordings of Heart rate (HR) in Cav1.3−/−, Cav3.1−/− and Cav1.3−/−/Cav3.1−/− mice. We studied the consequences of pharmacologic inhibition of f-HCN and TTX-sensitive Na+ channels in mutant mice using Langendorff perfused Hearts or optical mapping (OM) of the pacemaker impulse in intact SAN preparations (SANs). Results Cav ablation reduced HR in mice: Cav3.1−/− (−7.6%, n = 11), Cav1.3−/− (−24.4%, n = 8), Cav1.3−/−/Cav3.1−/− (−35%, n = 11). In OM experiments on SANs, concomitant inhibition of f-HCN and Nav1.1 channels slowed pacemaking in wild-type (−48%, n = 7) and Cav3.1−/− (−37%, n = 7), while arresting Automaticity in 4/6 of Cav1.3−/−, 3/6 of Cav1.3−/−/Cav3.1−/−. When present, residual pacemaking was reduced by 82%. Similar results were obtained using isolated Cav1.3−/−/Cav3.1−/− pacemaker cells were Automaticity arrested in 5/9 cells tested, or was reduced by 80% in 4/9 cells. Conclusion Heart Automaticity is primarily generated by Cav1.3 and f-HCN channels. RyR-dependent Ca2+ release cannot sustain Automaticity following concomitant targeting of Cav1.3 and f-HCN channels.
-
genesis and regulation of the Heart Automaticity
Physical Review, 2008Co-Authors: Matteo E Mangoni, Joel NargeotAbstract:The Heart Automaticity is a fundamental physiological function in higher organisms. The spontaneous activity is initiated by specialized populations of cardiac cells generating periodical electrica...
