Zobrazeno 1 - 10
of 10
pro vyhledávání: '"Jeffery Molkentin"'
Publikováno v:
Circulation. 144
Introduction: There is a lack of animal models of heart failure with preserved ejection fraction (HFpEF). Hypothesis: A mouse model with increased Ca2+ influx receiving a high-fat diet (HFD) and L-NAME (3 hits) could be a model for HFpEF to help reve
Publikováno v:
Circulation Research. 121
After MI, dead cardiomyocytes are permanently replaced by scar tissue mainly composed of fibroblasts and extracellular matrix (ECM) proteins due to the lack of cardiomyocyte regeneration. Previous attempts to characterize fibroblasts after MI were gr
Publikováno v:
Circulation Research. 111
Background: Protein phosphatase 1 is the major protein serine/threonine phosphatase in nearly all mammalian tissues, where it consists of three isoforms PP1α, PP1β, and PP1γ. However, the redundant or specific roles of each isoform in the heart is
Autor:
Qinghang Liu, Jeffery Molkentin
Publikováno v:
Circulation Research. 109
Both NFAT and NFkB are Rel homology domain-containing family members of transcription factors whose independent activities are critically involved in regulating cardiac hypertrophy and failure. Here we identified a novel transcriptional regulatory me
Autor:
Hongyu Zhang, Catherine Makarewich, Erhe Gao, Hajime Kubo, Hui Gao, Fang Wang, Remus Berretta, Walter Koch, Jeffery Molkentin, Steven Houser
Publikováno v:
Circulation Research. 109
The source of Ca 2+ to hypertrophic signaling after myocardial infarction (MI) is not clearly defined. Transient Receptor Potential Canonical (TRPC) channels could be an important source of hypertrophic Ca 2+ after MI. The objective of this study was
Autor:
Naser Jaleel, Hajime Kubo, Erhe Gao, Scott MacDonnell, Xiongwen Chen, Hiroyuki Nakayama, David Angert, Timothy Flynn, Remus Berretta, Hongyu Zhang, Walter Koch, Jeffery Molkentin, Steven Houser
Publikováno v:
Circulation. 118
Ca 2+ influx through L-type Ca 2+ channels (I Ca,L ) is essential for cardiac contraction and for activation of a variety of Ca 2+ dependent signaling pathways. However, Ca 2+ can also enter cardiac myocytes through T-type Ca 2+ channels (TTCCs), whi
Autor:
Thomas Force, Jeffery Molkentin
Publikováno v:
Principles of Molecular Medicine ISBN: 9781588292025
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::e7d75bf0b438d8aeb88b6bf820c3362f
https://doi.org/10.1007/978-1-59259-963-9_17
https://doi.org/10.1007/978-1-59259-963-9_17
Autor:
Hongyu Zhang, Xiongwen Chen, Erhe Gao, David Harris, Hiroyuki Nakayama, Xiaoying Zhang, scott Macdonnell, Andrea Eckhart, Walter Koch, Jeffery Molkentin, steven Houser
Publikováno v:
Circulation. 116
Myocyte death induced by ischemia or infarction can lead to depressed cardiac pump function and + inotropic drugs are often employed as therapy. The increased myocyte [Ca 2+ ] required to increase myocyte contractility can also induce cardiac hypertr
Publikováno v:
Circulation. 116
Thioredoxin1 (Trx1) reduces redox-sensitive proteins and regulates cell growth and death. We previously reported that cardiac hypertrophy induced by pressure-overload is suppressed in mice with cardiac specific overexpression of Trx1 (Tg-Trx1). To el
Autor:
Jeffery Molkentin
Publikováno v:
American Journal of Physiology-Endocrinology and Metabolism. 292:E367-E367