Výsledky vyhledávání - "Steven O. Marx"

Akademický článek

Multiple beta cell-independent mechanisms drive hypoglycemia in Timothy syndrome

Publikováno v: Nature Communications, Vol 15, Iss 1, Pp 1-14 (2024)

Abstract The canonical G406R mutation that increases Ca2+ influx through the CACNA1C-encoded CaV1.2 Ca2+ channel underlies the multisystem disorder Timothy syndrome (TS), characterized by life-threatening arrhythmias. Severe episodic hypoglycemia is

Externí odkaz: https://doaj.org/article/c69ae191aabc414ca794e63e3df33805

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Akademický článek

Effect of mechanical unloading on genome-wide DNA methylation profile of the failing human heart

Autor: Xianghai Liao, Peter J. Kennel, Bohao Liu, Trevor R. Nash, Richard Z. Zhuang, Amandine F. Godier-Furnemont, Chenyi Xue, Rong Lu, Paolo C. Colombo, Nir Uriel, Muredach P. Reilly, Steven O. Marx, Gordana Vunjak-Novakovic, Veli K. Topkara

Publikováno v: JCI Insight, Vol 8, Iss 4 (2023)

Heart failure (HF) is characterized by global alterations in myocardial DNA methylation, yet little is known about the epigenetic regulation of the noncoding genome and potential reversibility of DNA methylation with left ventricular assist device (L

Externí odkaz: https://doaj.org/article/56c323310ede495294a207d140e203cb

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Akademický článek

Increased Ca2+ influx through CaV1.2 drives aortic valve calcification

Autor: Maiko Matsui, Rihab Bouchareb, Mara Storto, Yasin Hussain, Andrew Gregg, Steven O. Marx, Geoffrey S. Pitt

Publikováno v: JCI Insight, Vol 7, Iss 5 (2022)

Calcific aortic valve disease (CAVD) is heritable, as revealed by recent GWAS. While polymorphisms linked to increased expression of CACNA1C — encoding the CaV1.2 L-type voltage-gated Ca2+ channel — and increased Ca2+ signaling are associated wit

Externí odkaz: https://doaj.org/article/3dfabf2342a344138338e463ae347f3a

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Akademický článek

Attenuating persistent sodium current–induced atrial myopathy and fibrillation by preventing mitochondrial oxidative stress

Publikováno v: JCI Insight, Vol 6, Iss 23 (2021)

Mechanistically driven therapies for atrial fibrillation (AF), the most common cardiac arrhythmia, are urgently needed, the development of which requires improved understanding of the cellular signaling pathways that facilitate the structural and ele

Externí odkaz: https://doaj.org/article/b7be647bfebd45409f3562f2a31b359c

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Akademický článek

Fibroblast growth factor homologous factors tune arrhythmogenic late NaV1.5 current in calmodulin binding–deficient channels

Autor: Jeffrey Abrams, Daniel Roybal, Nourdine Chakouri, Alexander N. Katchman, Richard Weinberg, Lin Yang, Bi-xing Chen, Sergey I. Zakharov, Jessica A. Hennessey, Uma Mahesh R. Avula, Johanna Diaz, Chaojian Wang, Elaine Y. Wan, Geoffrey S. Pitt, Manu Ben-Johny, Steven O. Marx

Publikováno v: JCI Insight, Vol 5, Iss 19 (2020)

The Ca2+-binding protein calmodulin has emerged as a pivotal player in tuning Na+ channel function, although its impact in vivo remains to be resolved. Here, we identify the role of calmodulin and the NaV1.5 interactome in regulating late Na+ current

Externí odkaz: https://doaj.org/article/efe44da0f05e4c1a960d684f11a8834d

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Rad regulation of CaV1.2 channels controls cardiac fight-or-flight response

Publikováno v: Nature Cardiovascular Research. 1:1022-1038

Fight-or-flight responses involve β-adrenergic-induced increases in heart rate and contractile force. In the present study, we uncover the primary mechanism underlying the heart’s innate contractile reserve. We show that four protein kinase A (PKA

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_________::d29a7152c7195aa5159ea1ac39befef0
https://doi.org/10.1038/s44161-022-00157-y

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Rad regulation of Ca

Publikováno v: Nature cardiovascular research. 1(11)

Fight-or-flight responses involve β-adrenergic-induced increases in heart rate and contractile force. In the present study, we uncover the primary mechanism underlying the heart's innate contractile reserve. We show that four protein kinase A (PKA)-

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=pmid________::098eb2ff6d51588c62d0ba69760229f2
https://pubmed.ncbi.nlm.nih.gov/36424916

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