Zobrazeno 1 - 10
of 19
pro vyhledávání: '"Emily K, Nguyen"'
Autor:
Olha M. Koval, Emily K. Nguyen, Dylan J. Mittauer, Karima Ait-Aissa, William C. Chinchankar, Isabella M. Grumbach
Publikováno v:
International Journal of Molecular Sciences, Vol 24, Iss 16, p 12897 (2023)
Type 2 diabetes (T2D) is associated with increased risk of atherosclerotic vascular disease due to excessive vascular smooth muscle cell (VSMC) proliferation. Here, we investigated the role of mitochondrial dysfunction and Ca2+ levels in VSMC prolife
Externí odkaz:
https://doaj.org/article/029ee44280c94cdbb8a60648414928d8
Autor:
Olha M. Koval, Emily K. Nguyen, Dylan J. Mittauer, Karima Ait-Aissa, William Chinchankar, Lan Qian, Muniswamy Madesh, Dao-Fu Dai, Isabella M. Grumbach
Publikováno v:
bioRxiv
BackgroundType 2 diabetes (T2D) is associated with a strongly increased risk for restenosis after angioplasty driven by proliferation of vascular smooth muscle cells (VSMCs). Here, we sought to determine whether and how mitochondrial dysfunction in T
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::0a1ca2a903f50fda58ba4c42cf8d2419
https://europepmc.org/articles/PMC9948984/
https://europepmc.org/articles/PMC9948984/
Autor:
Emily K. Nguyen, Promporn Suksaranjit, Mohammad A. Bashir, Dennis J. Firchau, Milena A. Gebska
Publikováno v:
JACC: Case Reports. 9:101533
Autor:
Paige Noble, William H. Thiel, Chantal Allamargot, Isabella M. Grumbach, Emily K. Nguyen, Stefan Strack, Meng Wu, Kim Broadhurst, Olha M. Koval
Publikováno v:
Arteriosclerosis, Thrombosis, and Vascular Biology. 38:1333-1345
Objective— The main objective of this study is to define the mechanisms by which mitochondria control vascular smooth muscle cell (VSMC) migration and impact neointimal hyperplasia. Approach and Results— The multifunctional CaMKII (Ca 2+ /calmodu
Autor:
Emily K. Nguyen, Isabella M. Grumbach
Publikováno v:
Arterioscler Thromb Vasc Biol
Mitochondria regulate major aspects of cell function by producing ATP, contributing to Ca 2+ signaling, influencing redox potential, and controlling levels of reactive oxygen species. In this review, we will discuss recent findings that illustrate ho
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::2db56868a2946e55ee042cea332d4750
https://europepmc.org/articles/PMC6531338/
https://europepmc.org/articles/PMC6531338/
Autor:
Olha M, Koval, Emily K, Nguyen, Velarchana, Santhana, Trevor P, Fidler, Sara C, Sebag, Tyler P, Rasmussen, Dylan J, Mittauer, Stefan, Strack, Prabhat C, Goswami, E Dale, Abel, Isabella M, Grumbach
Publikováno v:
Science signaling. 12(579)
The role of the mitochondrial Ca(2+) uniporter (MCU) in physiologic cell proliferation remains to be defined. Here, we demonstrated that the MCU was required to match mitochondrial function to metabolic demands during cell cycling. During the G1/S tr
Autor:
Prabhat C. Goswami, Emily K. Nguyen, Isabella M. Grumbach, Olha M. Koval, Velarchana Santhana, Stefan Strack, Trevor P. Fidler, Tyler P. Rasmussen, E. Dale Abel, Dylan J. Mittauer, Sara C. Sebag
Publikováno v:
Science Signaling. 12
The role of the mitochondrial Ca2+ uniporter (MCU) in physiologic cell proliferation remains to be defined. Here, we demonstrated that the MCU was required to match mitochondrial function to metabolic demands during the cell cycle. During the G1-S tr
Autor:
Emily K, Nguyen, Olha M, Koval, Paige, Noble, Kim, Broadhurst, Chantal, Allamargot, Meng, Wu, Stefan, Strack, William H, Thiel, Isabella M, Grumbach
Publikováno v:
Arteriosclerosis, thrombosis, and vascular biology. 38(6)
The main objective of this study is to define the mechanisms by which mitochondria control vascular smooth muscle cell (VSMC) migration and impact neointimal hyperplasia.The multifunctional CaMKII (CaThese findings identify mitochondrial CaMKII as a
Publikováno v:
Arteriosclerosis, Thrombosis, and Vascular Biology. 36
Background: Restenosis after angioplasty for coronary vascular disease remains a critical problem in cardiovascular medicine. Vascular smooth muscle cell (VSMC) migration and proliferation cause restenosis through neointima formation. Mitochondrial m
Autor:
Mark E. Anderson, Ashlee N. Venema, Isabella M. Grumbach, Elizabeth D. Luczak, Emily K. Nguyen, Megan E. Dibbern, Omar A. Jaffer, Xiaoqun Guan, Paula J. Klutho, Jason A. Scott, Linda J. Zhu, Anand Prasad, Litao Xie
Publikováno v:
Vascular pharmacology. 60(2)
Activation of the Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) and reactive oxygen species (ROS) promote neointimal hyperplasia after vascular injury. CaMKII can be directly activated by ROS through oxidation. In this study, we determined w