scholarly journals LIN28a induced metabolic and redox regulation promotes cardiac cell survival in the heart after ischemic injury

Redox Biology ◽  
2021 ◽  
Vol 47 ◽  
pp. 102162
Author(s):  
Antonia Elizabeth Yuko ◽  
Vagner Oliveira Carvalho Rigaud ◽  
Justin Kurian ◽  
Ji H. Lee ◽  
Nicole Kasatkin ◽  
...  
2015 ◽  
Vol 2015 ◽  
pp. 1-11 ◽  
Author(s):  
Juhyun Song ◽  
Joohyun Park ◽  
Yumi Oh ◽  
Jong Eun Lee

Ischemic stroke interrupts the flow of blood to the brain and subsequently results in cerebral infarction and neuronal cell death, leading to severe pathophysiology. Glutathione (GSH) is an antioxidant with cellular protective functions, including reactive oxygen species (ROS) scavenging in the brain. In addition, GSH is involved in various cellular survival pathways in response to oxidative stress. In the present study, we examined whether GSH reduces cerebral infarct size after middle cerebral artery occlusionin vivoand the signaling mechanisms involved in the promotion of cell survival after GSH treatment under ischemia/reperfusion conditionsin vitro. To determine whether GSH reduces the extent of cerebral infarction, cell death after ischemia, and reperfusion injury, we measured infarct size in ischemic brain tissue and the expression of claudin-5 associated with brain infarct formation. We also examined activation of the PI3K/Akt pathway, inactivation of FOXO3, and expression of Bcl2 to assess the role of GSH in promoting cell survival in response to ischemic injury. Based on our results, we suggest that GSH might improve the pathogenesis of ischemic stroke by attenuating cerebral infarction and cell death.


2013 ◽  
Vol 45 (8) ◽  
pp. 1577-1584 ◽  
Author(s):  
Zhelong Xu ◽  
SungRyul Lee ◽  
Jin Han

2005 ◽  
Vol 59 (4) ◽  
pp. 197-203 ◽  
Author(s):  
T. Galeotti ◽  
G. Pani ◽  
C. Capone ◽  
B. Bedogni ◽  
S. Borrello ◽  
...  

2009 ◽  
Vol 11 (11) ◽  
pp. 2741-2758 ◽  
Author(s):  
Md. Kaimul Ahsan ◽  
Istvan Lekli ◽  
Diptarka Ray ◽  
Junji Yodoi ◽  
Dipak K. Das

2010 ◽  
Vol 107 (4) ◽  
pp. 448-450 ◽  
Author(s):  
Yaron Aviv ◽  
Lorrie A. Kirshenbaum
Keyword(s):  

2009 ◽  
Vol 96 (3) ◽  
pp. 273a
Author(s):  
Irina Korichneva ◽  
Helen Khanova ◽  
Nashaba Khan ◽  
Camie Doyle

2008 ◽  
Vol 15 (5) ◽  
pp. 867-878 ◽  
Author(s):  
E Giannoni ◽  
F Buricchi ◽  
G Grimaldi ◽  
M Parri ◽  
F Cialdai ◽  
...  

2010 ◽  
Vol 86 (1) ◽  
pp. 1-3
Author(s):  
D. Li ◽  
C. Depre
Keyword(s):  

2019 ◽  
Vol 18 ◽  
pp. 153303381986431
Author(s):  
Wenqiao Jia ◽  
Pengxiang Chen ◽  
Yufeng Cheng

Reactive oxygen species play a vital role in cell survival by regulating physiological metabolism and signal transduction of cells. The imbalance of oxidant and antioxidant states induces oxidative stress within a cell. Redox regulation and oxidative stress are closely related to survival and proliferation of stem cells, cancer cells, and cancer stem cells. Peroxiredoxin 4, a typical endoplasmic reticulum-resident 2-Cys antioxidant of peroxiredoxins, can fine-tune hydrogen peroxide catabolism which affects cell survival by affecting redox balance, oxidative protein folding, and regulation of hydrogen peroxide signaling. Recent studies revealed the overexpression of peroxiredoxin 4 in several kinds of cancers, such as breast cancer, prostate cancer, ovarian cancer, colorectal cancer, and lung cancer. And it has been demonstrated that peroxiredoxin 4 causally contributes to tumorigenesis, therapeutic resistance, metastasis, and recurrence of tumors. In this article, the characteristics of peroxiredoxin 4 in physiological functions and the cancer-related research progress of mammalian peroxiredoxin 4 is reviewed. We believe that peroxiredoxin 4 has the potential of serving as a novel target for multiple cancers.


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