Zobrazeno 1 - 10
of 513
pro vyhledávání: '"S. Janicki"'
Autor:
Yifan Xing, Ting Niu, Wenjuan Wang, Jinqing Li, Siying Li, Joseph S Janicki, Stacey Ruiz, Colin J Meyer, Xing Li Wang, Dongqi Tang, Yuxia Zhao, Taixing Cui
Publikováno v:
PLoS ONE, Vol 19, Iss 11, p e0314793 (2024)
[This corrects the article DOI: 10.1371/journal.pone.0044899.].
Externí odkaz:
https://doaj.org/article/42d00c265a114282a02ced998314b5ce
Autor:
Heather M. Dehlin, Edward J. Manteufel, Alexander Widiapradja, Bao Lu, Scott P. Levick, Lauren L. Kolb, Joseph S. Janicki, James R. Peña, Paul H. Goldspink, Amit Sharma, John D. Imig
Publikováno v:
Scientific Reports, Vol 9, Iss 1, Pp 1-11 (2019)
Scientific Reports
Scientific Reports
Cardiac fibrosis is an underlying cause of diastolic dysfunction, contributing to heart failure. Substance P (SP) activation of the neurokinin-1 receptor (NK-1R) contributes to cardiac fibrosis in hypertension. However, based on in vitro experiments,
Publikováno v:
Analysis and Simulation of the Cardiac System — Ischemia ISBN: 9781003068341
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::e194b579c31b43439fe73caaed7950b5
https://doi.org/10.4324/9781003068341-35
https://doi.org/10.4324/9781003068341-35
Autor:
Yifan Xing, Ting Niu, Wenjuan Wang, Jinqing Li, Siying Li, Joseph S Janicki, Stacey Ruiz, Colin J Meyer, Xing Li Wang, Dongqi Tang, Yuxia Zhao, Taixing Cui
Publikováno v:
PLoS ONE, Vol 7, Iss 9, p e44899 (2012)
Nuclear factor E2-related factor 2 (Nrf2) appears to be an attractive therapeutic target for the treatment of cardiac disease. We investigated whether a synthetic triterpenoid derivative of dihydro-CDDO-trifluoroethylamide (dh404), a novel Nrf2 activ
Externí odkaz:
https://doaj.org/article/39ceeed1d530494f8c81c05448eb196c
Publikováno v:
PLoS ONE, Vol 4, Iss 12, p e8391 (2009)
Targeting Nrf2 signaling appears to be an attractive approach for the treatment of maladaptive cardiac remodeling and dysfunction; however, pharmacological modulation of the Nrf2 pathway in the cardiovascular system remains to be established. Herein,
Externí odkaz:
https://doaj.org/article/66fc5dd01b224c0f83669f1b7b400c41
Nrf2-Mediated Cardiac Maladaptive Remodeling and Dysfunction in a Setting of Autophagy Insufficiency
Autor:
Joseph S. Janicki, Lei Qi, Ting Niu, Mitzi Nagarkatti, Xuejun Wang, Huimei Zang, Xing Li Wang, Linmao Lyu, Qingyun Qin, Chen Qu, Prakash S. Nagarkatti, Taixing Cui
Publikováno v:
Hypertension. 67:107-117
Nuclear factor erythroid-2–related factor 2 (Nrf2) appears to exert either a protective or detrimental effect on the heart; however, the underlying mechanism remains poorly understood. Herein, we uncovered a novel mechanism for turning off the Nrf2
Autor:
Dongqi Tang, Yimu Lai, Joseph S. Janicki, Xing Li Wang, Sao Cong Sun, Bin Li, Siying Li, Haibo Song, Wenjuan Wang, Taixing Cui, Hui Wang, Chen Qu, Bryan J. Mathis, Lei Shao
Publikováno v:
Journal of Molecular and Cellular Cardiology. 84:143-153
Ubiquitin proteasome system (UPS) consists of ubiquitin, ubiquitin-activating enzymes (E1s), ubiquitin-conjugating enzymes (E2s), ubiquitin ligases (E3s), proteasomes, and deubiquitinating enzymes (DUBs). Ubiquitin, E1s, several E2s, E3s, and proteas
Autor:
Yimu Lai, Mitzi Nagarkatti, Xing-Song Tian, Hechu Li, Taixing Cui, Lorne J. Hofseth, Xing Li Wang, Chen Qu, Prakash S. Nagarkatti, Anthony Windust, Bin Li, Joseph S. Janicki, Dongqi Tang
Publikováno v:
Journal of Ethnopharmacology. 168:326-336
Ethnopharmacological relevance: American ginseng is capable of ameliorating cardiac dysfunction and activating Nrf2, a master regulator of antioxidant defense, in the heart. This study was designed to isolate compounds from American ginseng and to de
Publikováno v:
Current Drug Targets. 16:284-294
The conserved cylindromatosis (CYLD) codes for a deubiquitinating enzyme and is a crucial regulator of diverse cellular processes such as immune responses, inflammation, death, and proliferation. It directly regulates multiple key signaling cascades,
Publikováno v:
Hypertension. 65:328-334
Estrogen regulation of myocardial chymase and chymase effects on cardiac remodeling are unknown. To test the hypothesis that estrogen prevents pressure overload–induced adverse cardiac remodeling by inhibiting mast cell (MC) chymase release, transv