scholarly journals Therapeutic Potential of Peroxisome Proliferators–Activated Receptor-α/γ Dual Agonist With Alleviation of Endoplasmic Reticulum Stress for the Treatment of Diabetes

Diabetes ◽  
2007 ◽  
Vol 57 (3) ◽  
pp. 737-745 ◽  
Author(s):  
Kyu Lee Han ◽  
Joo Sun Choi ◽  
Jae Young Lee ◽  
Jihyun Song ◽  
Myung Kuk Joe ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Therapeutic Potential ◽  
Peroxisome Proliferators ◽  
Treatment Of Diabetes ◽  
Dual Agonist

Regulatory effects of ghrelin on endoplasmic reticulum stress, oxidative stress, and autophagy: Therapeutic potential

Neuropeptides ◽  
2021 ◽  
Vol 85 ◽  
pp. 102112
Author(s):  
Huiqing Wang ◽  
Shanshan Dou ◽  
Junge Zhu ◽  
Ziqi Shao ◽  
Chunmei Wang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Therapeutic Potential ◽  
Regulatory Effects ◽  
Stress Oxidative

scholarly journals The antitumour drug ABTL0812 impairs neuroblastoma growth through endoplasmic reticulum stress-mediated autophagy and apoptosis

2020 ◽  
Vol 11 (9) ◽  
Author(s):  
Laia París-Coderch ◽  
Aroa Soriano ◽  
Carlos Jiménez ◽  
Tatiana Erazo ◽  
Pau Muñoz-Guardiola ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Cell Death ◽  
High Risk ◽  
Endoplasmic Reticulum Stress ◽  
Therapeutic Potential ◽  
Antitumour Activity ◽  
Neuroblastoma Cell ◽  
Genetic Alterations ◽  
Alternative Pathways ◽  
Cancer Cell Death

Abstract Neuroblastoma is the leading cause of cancer death in children aged 1 to 4 years. Particularly, five-year overall survival for high-risk neuroblastoma is below 50% with no curative options when refractory or relapsed. Most of current therapies target cell division and proliferation, thereby inducing DNA damage and programmed cell death. However, aggressive tumours often present alterations of these processes and are resistant to therapy. Therefore, exploring alternative pathways to induce tumour cell death will provide new therapeutic opportunities for these patients. In this study we aimed at testing the therapeutic potential of ABTL0812, a novel anticancer drug that induces cytotoxic autophagy to eliminate cancer cells, which is currently in phase II clinical trials of adult tumours. Here, we show that ABTL0812 impaired the viability of clinical representative neuroblastoma cell lines regardless of genetic alterations associated to bad prognosis and resistance to therapy. Oral administration of ABTL0812 to mice bearing neuroblastoma xenografts impaired tumour growth. Furthermore, our findings revealed that, in neuroblastoma, ABTL0812 induced cancer cell death via induction of endoplasmic reticulum stress, activation of the unfolded protein response, autophagy and apoptosis. Remarkably, ABTL0812 potentiated the antitumour activity of chemotherapies and differentiating agents such as irinotecan and 13-cis-retinoic acid. In conclusion, ABTL0812 distinctive mechanism of action makes it standout to be used alone or in combination in high-risk neuroblastoma patients.

Endoplasmic reticulum stress in disease: mechanisms and therapeutic opportunities

2009 ◽  
Vol 118 (1) ◽  
pp. 19-29 ◽  
Author(s):  
Toru Hosoi ◽  
Koichiro Ozawa
Keyword(s):  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Neurodegenerative Diseases ◽  
Er Stress ◽  
Therapeutic Potential ◽  
Unfolded Protein ◽  
Pathological Conditions ◽  
Disease Mechanisms ◽  
Obesity And Diabetes ◽  
Protein Response

Various stresses, which impair ER (endoplasmic reticulum) function, lead to an accumulation of unfolded or misfolded proteins. ER stress triggers many rescuer responses, including a UPR (unfolded protein response). Increasing evidence has suggested that ER stress is involved in neurodegenerative diseases (Alzheimer's disease, Parkinson's disease and cerebral ischaemic insults), cancer, obesity and diabetes. In the present review, we consider the importance of ER stress under pathological conditions in mammals. Furthermore, we discuss the therapeutic potential for treatment targeting ER stress.

Abstract #403: The Glutathione Mimic Ebselen Inhibits Oxidative Stress but not Endoplasmic Reticulum Stress in Endothelial Cells.

2015 ◽  
Vol 21 ◽  
pp. 85-86
Author(s):  
William Kurban ◽  
Salma Makhoul Ahwach ◽  
Melanie Thomas ◽  
Luisa Onsteed-Haas ◽  
Michael Haas
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cells ◽  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress
Sign in / Sign up

Export Citation Format

Share Document