The endoplasmic reticulum is the site of cholesterol-induced cytotoxicity in macrophages

By Bo Feng, P. M. Yao, Yankun Li, C. Devlin, Da-jun Zhang, H. Harding, M. Sweeney, J. Rong, G. Kuriakose, E. Fisher and 3 more. Nature Cell Biology, 2003

916 citations recorded by the source corpus.

Subfields: Cell Biology, Epidemiology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/0e6911fb61f4cc9f25f1821cf7a63a93fd3bc600

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. G. Hotamışlıgil
2. R. Kaufman
3. D. Ron
4. H. Harding
5. S. Oyadomari
6. S. Marciniak
7. I. Novoa
8. Yuhong Zhang

In Epidemiology

1. R. Kaufman
2. D. Ron
3. G. Hotamışlıgil
4. H. Harding
5. I. Novoa
6. I. Tabas
7. S. Oyadomari
8. Yuhong Zhang

In Molecular Biology

1. G. Hotamışlıgil
2. D. Ron
3. R. Kaufman
4. H. Harding
5. I. Novoa
6. Yuhong Zhang
7. S. Marciniak
8. S. Oyadomari

Citations in the corpus

• Nutrient sensing and inflammation in metabolic diseases (2008, background): “For example, in macrophages, accumulation of free cholesterol leads to apoptosis through the activation of the ER stress response and JN”
• CHOP induces death by promoting protein synthesis and oxidation in the stressed endoplasmic reticulum. (2004, background): “2002), free cholesterol loading of macrophages in atherosclerotic lesions (Feng et al. 2003), and even -cell exhaustion in Diabetes Mellitus (Oyadomari et al.”
• Cellular cholesterol trafficking and compartmentalization (2008, background): “, the activity of resident ER proteins and the exit of newly synthesized membrane proteins from the E”
• Endoplasmic Reticulum Stress and Oxidative Stress: A Vicious Cycle or a Double-Edged Sword? (2007, neutral): “Recent findings suggest that free cholesterol requires trafficking to the ER to produce its toxic effects (29).”
• Lipid signalling in disease (2008, background): “The accumulation of excess lipid, in particular saturated fatty acids and sterols, might induce cellular damage through stress on the membranes of lipid-metabolizing organelles, especially the endoplasmic reticulum (ER) and possibly mitochondri”
• Cholesterol induces CD8+ T-cell exhaustion in the tumor microenvironment (2019, positive): “Excess cellular cholesterol induces the unfolded protein response in the ER and results in ER stress (Devries-Seimon et al., 2005; Feng et al., 2003).”
• Measuring ER stress and the unfolded protein response using mammalian tissue culture system (2011, methodology): “Acetyl-LDL (100 mg/ml) plus the acyl-CoA:cholesterol acyltransferase inhibitor 58035 induces ER stress in macrophages in 5–10 h (Feng et al., 2003).”
• Initiation and execution of lipotoxic ER stress in pancreatic β-cells (2008, methodology): “…chemical JNK inhibitor SP600125 (Merck-Calbiochem) was dissolved in DMSO, and the peptide JNK inhibitor L-TAT-JNKi (a kind gift of C. Bonny and M. Mathieu; XigenPharma, Lausanne, Switzerland) was dissolved in culture medium at concentrations previously used (Bonny et al., 2001; Ozcan et al., 2004).”
• Endoplasmic reticulum stress signaling in disease. (2006, background): “Indeed, recent findings indicate that for free cholesterol to have its toxic effect it must be trafficked to the ER (45).”
• Membrane lipid saturation activates endoplasmic reticulum unfolded protein response transducers through their transmembrane domains (2013, background): “Enhanced UPR signaling has been observed in cholesterol-loaded macrophages (9), in pancreatic beta cells exposed to saturated fatty acids (10), and in the liver of mice fed a high-fat diet (11) and is believed to play a role in the lipotoxicity associated with obesity and type II diabetes mellitus.”