Integrating the mechanisms of apoptosis induced by endoplasmic reticulum stress

By I. Tabas, D. Ron. Nature Cell Biology, 2011

2,569 citations recorded by the source corpus.

The ability to respond to perturbations in endoplasmic reticulum (ER) function is a fundamentally important property of all cells, but ER stress can also lead to apoptosis. In settings of chronic ER stress, the associated apoptosis may contribute to pathophysiological processes involved in a number of prevalent diseases, including neurodegenerative diseases, diabetes, atherosclerosis and renal disease. The molecular mechanisms linking ER stress to apoptosis are the topic of this review, with emphases on relevance to pathophysiology and integration and complementation among the various apoptotic pathways induced by ER stress.

Subfields: Cell Biology, Epidemiology, Surgery

View Paper: https://www.semanticscholar.org/paper/a8616e633f9ebb62a5df5ab8a5f8b6cc22a85bc2

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cell Biology

1. R. Kaufman
2. S. S. Cao
3. I. Tabas
4. Afshin Samali
5. Peter Walter
6. K. Bornfeldt
7. C. Hetz
8. Michael D. Blower

In Epidemiology

1. R. Kaufman
2. K. Bornfeldt
3. Afshin Samali
4. S. S. Cao
5. I. Tabas
6. Peter Walter
7. Han Li
8. A. Suomalainen

In Surgery

1. R. Kaufman
2. K. Bornfeldt
3. S. S. Cao
4. Peter Walter
5. Michael D. Blower
6. I. Tabas
7. D. Schwarz
8. Afshin Samali

Citations in the corpus

• Endoplasmic Reticulum Stress and Oxidative Stress in Cell Fate Decision and Human Disease (2014, background): “In addition, CHOP can activate transcription of other pro-apoptotic genes, including telomere repeat binding factor 3 (TRB3) and death receptor 5 (DR5), both of which are important mediators of ER stress-induced apoptosis in several cancer cells (161).”
• Endoplasmic reticulum stress sensing in the unfolded protein response. (2013, background): “ER stress-induced apoptosis is an important pathogenic factor in a number of widespread diseases, including diabetes , neurodegenerative diseases, atherosclerosis , and renal disease (Tabas and Ron 2011).”
• The endoplasmic reticulum: structure, function and response to cellular signaling (2015, background): “If the balance is not restored it can lead to cell death or apoptosis [147], therefore achieving normal function is critical to the survival of the cell.”
• Impairment of ceramide synthesis causes a novel progressive myoclonus epilepsy (2014, background): “ATF4/PERK signaling controls the transcription of C/EBP-homologous protein (CHOP), a critical factor promoting mitochondria-dependent apoptosis through the transcriptional regulation of the BCL-2 protein family.(15) Intriguingly, in CerS1-silenced Neuro2A cells, CHOP transcripts significantly increa”
• PERK is required at the ER-mitochondrial contact sites to convey apoptosis after ROS-based ER stress (2012, background): “However, when chronic or too severe, ER stress will engage apoptosis.(2,3) Recently, reactive oxygen species (ROS) have emerged as crucial regulators of ER function and UPR activation and in several diseased conditions, ER stress and increased ROS production occur concurrently.”
• The Cellular Biology of Macrophages in Atherosclerosis (2011, neutral): “The UPR functions in normal physiology to correct disequilibria in ER function, but when ER stress is abnormally prolonged, persistent expression of the UPR effector C/EBP-homologous protein (CHOP) can trigger apoptosis (Tabas and Ron, 2011).”
• Pharmacological brake-release of mRNA translation enhances cognitive memory (2013, background): “Although the UPR initially mitigates ER stress and as such confers cytoprotection, persistent and severe ER stress leads to activation of apoptosis that eliminates damaged cells (Shore et al., 2011; Tabas and Ron, 2011).”
• The C/EBP Homologous Protein (CHOP) Transcription Factor Functions in Endoplasmic Reticulum Stress-Induced Apoptosis and Microbial Infection (2019, background): “CHOP deficient mouse experiments revealed that CHOP-induced apoptosis is relevant to many diseases that cause ER stress (22, 23).”
• Mitochondria: In Sickness and in Health (2012, background): “Ca2+ release at ER-mitochondrial contacts may sensitize mitochondria to apoptotic effectors (Breckenridge et al., 2003; Iwasawa et al., 2011; Tabas and Ron, 2011).”
• Insulin Resistance, Hyperglycemia, and Atherosclerosis (2011, positive): “…mechanism is likely relevant to the recent finding that CHOP promotes macrophage apoptosis by stimulating the release of calcium from the ER, which subsequently activates an apoptosis execution program coordinated by calcium/calmodulin-dependent protein kinase II (CaMKII) (Tabas and Ron, 2011).”