Zobrazeno 1 - 10
of 17
pro vyhledávání: '"Jason K. Higa"'
Autor:
Briana K. Shimada, Naaiko Yorichika, Jason K. Higa, Yuichi Baba, Motoi Kobayashi, Toshinori Aoyagi, Tomohiro Suhara, Takashi Matsui
Publikováno v:
Physiological Reports, Vol 9, Iss 6, Pp n/a-n/a (2021)
Abstract The mechanistic target of rapamycin (mTOR) is a key mediator of energy metabolism, cell growth, and survival. While previous studies using transgenic mice with cardiac‐specific overexpression of mTOR (mTOR‐Tg) demonstrated the protective
Externí odkaz:
https://doaj.org/article/042ba68a7c4741258784f2e28684b7b3
The Role of Ferroptosis in Adverse Left Ventricular Remodeling Following Acute Myocardial Infarction
Publikováno v:
Cells, Vol 11, Iss 9, p 1399 (2022)
Ferroptosis is an iron-dependent form of regulated cell death and is distinct from other conventional forms of regulated cell death. It is often characterized by the dysfunction of the antioxidant selenoprotein glutathione peroxidase 4 (GPX4) antioxi
Externí odkaz:
https://doaj.org/article/7032bad51aba4ad09e89a5e43ed202e1
Autor:
Sumit Kar, Shi Su, Nicholas K. Kawasaki, Takashi Matsui, Adriana Adameova, Paras Kumar Mishra, James M. Downey, Jagat Narula, Peter M. Kang, Joseph A. Hill, Christopher P. Baines, Antonio Abbate, Hande Piristine, Jason K. Higa, Masafumi Takahashi
Publikováno v:
Am J Physiol Heart Circ Physiol
Cell death is a fundamental process in cardiac pathologies. Recent studies have revealed multiple forms of cell death, and several of them have been demonstrated to underlie adverse cardiac remodeling and heart failure. With the expansion in the area
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::68f9982c52521ae13f42e75eb19e78c5
https://doi.org/10.1152/ajpheart.00259.2019
https://doi.org/10.1152/ajpheart.00259.2019
Autor:
Tomohiro Suhara, Takashi Matsui, Yuichi Baba, Motoi Kobayashi, Jason K. Higa, Briana K. Shimada, Naaiko Yorichika, Toshinori Aoyagi
Publikováno v:
Physiological Reports
Physiological Reports, Vol 9, Iss 6, Pp n/a-n/a (2021)
Physiological Reports, Vol 9, Iss 6, Pp n/a-n/a (2021)
The mechanistic target of rapamycin (mTOR) is a key mediator of energy metabolism, cell growth, and survival. While previous studies using transgenic mice with cardiac‐specific overexpression of mTOR (mTOR‐Tg) demonstrated the protective effects
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::55be5d0df7fab61a3e45af1bf89fbfff
https://doi.org/10.14814/phy2.14807
https://doi.org/10.14814/phy2.14807
Autor:
Motoi Kobayashi, Takashi Matsui, Tomohiro Suhara, Yuichi Baba, Jason K. Higa, Nicholas K. Kawasaki
Publikováno v:
Current Drug Targets. 19:1068-1076
Iron is an essential mineral required for a variety of vital biological functions. Despite being vital for life, iron also has potentially toxic aspects. Iron has been investigated as a risk factor for coronary artery disease (CAD), however, iron's t
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::caf3175a2464fdea048dc589bf89657d
https://doi.org/10.2174/1389450119666180605112235
https://doi.org/10.2174/1389450119666180605112235
Autor:
Takashi Matsui, Hiroko Aoyagi, Briana K. Shimada, Kate M. Horiuchi, Motoi Kobayashi, Hiroaki Kitaoka, Yuichi Baba, Tomohiro Suhara, Jonathan D. Woo, Jason K. Higa, Karra S. Marh
Publikováno v:
American Journal of Physiology-Heart and Circulatory Physiology. 314:H659-H668
Clinical studies have suggested that myocardial iron is a risk factor for left ventricular remodeling in patients after myocardial infarction. Ferroptosis has recently been reported as a mechanism of iron-dependent nonapoptotic cell death. However, f
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::9c2ff22e0e9f5a7821aa687d2e4a19b4
https://doi.org/10.1152/ajpheart.00452.2017
https://doi.org/10.1152/ajpheart.00452.2017
Publikováno v:
American journal of physiology. Heart and circulatory physiology. 316(3)
β-Adrenergic receptor (β-AR) stimulation increases extracellular levels of ubiquitin (UB) in myocytes, and exogenous UB decreases β-AR-stimulated myocyte apoptosis and myocardial fibrosis. Here, we hypothesized that exogenous UB modulates the infl
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::a1d4584409baa84d4f1704da6d21a8c6
https://pubmed.ncbi.nlm.nih.gov/30681370
https://pubmed.ncbi.nlm.nih.gov/30681370
Publikováno v:
Ferroptosis in Health and Disease ISBN: 9783030267797
Ferroptosis is a relatively newly discovered form of cell death, and although studies confirm its mechanisms in a variety of tissues and diseases, few studies confirm its mechanisms in the heart. The heart depends on iron for its constant energy dema
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::89f3757969105efb799aa7e442156df9
https://doi.org/10.1007/978-3-030-26780-3_9
https://doi.org/10.1007/978-3-030-26780-3_9
Publikováno v:
Curr Diab Rep
PURPOSE OF REVIEW: Type 2 diabetes mellitus (T2DM) is a risk factor for heart failure. The mechanistic target of rapamycin (mTOR) is a key mediator of the insulin signaling pathway. We will discuss the role of mTOR in myocardial dysfunction in T2DM.
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::811e60a7d97f0b4dc6bc10e2cb600c5c
https://europepmc.org/articles/PMC8219468/
https://europepmc.org/articles/PMC8219468/
Autor:
Jagat Narula, Paras Kumar Mishra, Shi Su, Antonio Abbate, James M. Downey, Hande Piristine, Peter M. Kang, Jason K. Higa, Sumit Kar, Takashi Matsui, Masafumi Takahashi, Adriana Adameova, Christopher P. Baines, Nicholas K. Kawasaki, Joseph A. Hill
Publikováno v:
American Journal of Physiology-Heart and Circulatory Physiology. 317:H1390-H1390
Cell death is a fundamental process in cardiac pathologies. Recent studies have revealed multiple forms of cell death, and several of them have been demonstrated to underlie adverse cardiac remodeling and heart failure. With the expansion in the area
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::64bde959f995b32b1a9a4ef0067a5feb
https://doi.org/10.1152/ajpheart.zh4-2975-corr.2019
https://doi.org/10.1152/ajpheart.zh4-2975-corr.2019