Zobrazeno 1 - 10
of 148
pro vyhledávání: '"Jin O‐Uchi"'
Publikováno v:
Physiological Reports, Vol 12, Iss 6, Pp n/a-n/a (2024)
Abstract Cardiac fibroblasts (CFs) are an attractive target for reducing pathological cardiac remodeling, and understanding the underlying mechanisms of these processes is the key to develop successful therapies for treating the pressure‐overloaded
Externí odkaz:
https://doaj.org/article/cba148bde38f493782151afd489ec03e
Autor:
Alexander Vang, Denielli da Silva Gonçalves Bos, Ana Fernandez-Nicolas, Peng Zhang, Alan R. Morrison, Thomas J. Mancini, Richard T. Clements, Iuliia Polina, Michael W. Cypress, Bong Sook Jhun, Edward Hawrot, Ulrike Mende, Jin O-Uchi, Gaurav Choudhary
Publikováno v:
JCI Insight, Vol 6, Iss 12 (2021)
Right ventricular (RV) fibrosis is a key feature of maladaptive RV hypertrophy and dysfunction and is associated with poor outcomes in pulmonary hypertension (PH). However, mechanisms and therapeutic strategies to mitigate RV fibrosis remain unrealiz
Externí odkaz:
https://doaj.org/article/c09c89c74fdf402a92c4c34005193f3d
Enhancing Autophagy Diminishes Aberrant Ca2+ Homeostasis and Arrhythmogenesis in Aging Rabbit Hearts
Autor:
Kevin R. Murphy, Brett Baggett, Leroy L. Cooper, Yichun Lu, Jin O-Uchi, John M. Sedivy, Dmitry Terentyev, Gideon Koren
Publikováno v:
Frontiers in Physiology, Vol 10 (2019)
AimAging in humans is associated with a 10–40-fold greater incidence of sudden cardiac death from malignant tachyarrhythmia. We have reported that thiol oxidation of ryanodine receptors (RyR2s) by mitochondria-derived reactive oxygen species (mito-
Externí odkaz:
https://doaj.org/article/28f8dbb9fc3242e4974f494ea275273f
Publikováno v:
Frontiers in Cardiovascular Medicine, Vol 6 (2019)
Externí odkaz:
https://doaj.org/article/5a05a72408cf43578a93925c1e237a11
Autor:
Shanna Hamilton, Radmila Terentyeva, Tae Yun Kim, Peter Bronk, Richard T. Clements, Jin O-Uchi, György Csordás, Bum-Rak Choi, Dmitry Terentyev
Publikováno v:
Frontiers in Physiology, Vol 9 (2018)
In a physiological setting, mitochondria increase oxidative phosphorylation during periods of stress to meet increased metabolic demand. This in part is mediated via enhanced mitochondrial Ca2+ uptake, an important regulator of cellular ATP homeostas
Externí odkaz:
https://doaj.org/article/afd9fd2a470d40ac8bbdb50a6b5dfb09
Autor:
Tomas Rajtik, Slavka Carnicka, Adrian Szobi, Zoltan Giricz, Jin O-Uchi, Veronika Hassova, Pavel Svec, Peter Ferdinandy, Tanya Ravingerova, Adriana Adameova
Publikováno v:
Data in Brief, Vol 7, Iss , Pp 730-734 (2016)
Content of particular proteins indicating cellular injury due to apoptosis and necrosis has been investigated in ischemic/reperfused (IR) hearts and ischemic/reperfused hearts treated with CaMKII inhibitor and/or AT1 receptor inhibitor. This data art
Externí odkaz:
https://doaj.org/article/7a49268a8081425485b908240be473ac
Publikováno v:
Antioxidants, Vol 7, Iss 12, p 195 (2018)
Abnormal mitochondrial morphology, especially fragmented mitochondria, and mitochondrial dysfunction are hallmarks of a variety of human diseases including heart failure (HF). Although emerging evidence suggests a link between mitochondrial fragmenta
Externí odkaz:
https://doaj.org/article/fa0dfa4e2350449e9027708dc95be1d6
Autor:
Felipe Kazmirczak, Lynn M. Hartweck, Neal T. Vogel, Jenna B. Mendelson, Anna K. Park, Rashmi M. Raveendran, Jin O-Uchi, Bong Sook Jhun, Sasha Z. Prisco, Kurt W. Prins
Publikováno v:
JACC Basic Transl Sci
Intermittent fasting (IF) extends life span via pleotropic mechanisms, but one important molecular mediator is adenosine monophosphate–activated protein kinase (AMPK). AMPK enhances lipid metabolism and modulates microtubule dynamics. Dysregulation
Publikováno v:
Physiology. 38
Introduction: Mechanical stress (e.g., pressure overload), cytokines, growth factors, and neurohumoral mediators stimulate cardiac fibroblast (CF) activation, which promotes extracellular matrix (ECM) protein synthesis leading to cardiac fibrosis and
Publikováno v:
Physiology. 38
Introduction: Direct infection and viral protein expression of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) in the respiratory system, and other organs including the heart, contribute to multi-organ dysfunction during COVID-19. We pre