Homocysteine-induced endoplasmic reticulum stress causes dysregulation of the cholesterol and triglyceride biosynthetic pathways.

By G. Werstuck, S. Lentz, S. Dayal, G. Hossain, S. Sood, Yuan-Yuan Shi, Ji Zhou, N. Maeda, S. Krisans, M. Malinow and 1 more. Journal of Clinical Investigation, 2001

729 citations recorded by the source corpus.

Subfields: Cell Biology, Epidemiology, Rheumatology

View Paper: https://www.semanticscholar.org/paper/3ef533f6d1eb806600c634bd1e6a7f7220154151

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. J. Malhotra
3. D. Ron
4. Min Ni
5. S. Marciniak
6. H. Chae
7. Hyung-Ryong Kim
8. M. Cnop

In Epidemiology

1. R. Kaufman
2. J. Malhotra
3. Min Ni
4. D. Ron
5. Amy S. Lee
6. H. Chae
7. Hyung-Ryong Kim
8. F. Foufelle

Citations in the corpus

• Endoplasmic Reticulum Stress and Oxidative Stress: A Vicious Cycle or a Double-Edged Sword? (2007, positive): “In addition, over-expression of BiP prevented SREBP induction in response to homocysteine (149).”
• Orchestrating the unfolded protein response in health and disease. (2002, background): “SREBP cleavage, leading to intracellular accumulation of cholesterol (77).”
• Hepatic steatosis: a role for de novo lipogenesis and the transcription factor SREBP‐1c (2010, background): “Homocysteine induces ER stress concomitant with the activation of SREBP in cultured human hepatocytes and in vascular endothelial cells [69].”
• Endoplasmic reticulum stress signaling in disease. (2006, background): “The likely explanation is local lipid synthesis, and consistent with this, homocysteine has been shown to activate lipogenic signaling via the sterol regulated element-binding proteins (SREBPs) (205).”
• ER chaperones in mammalian development and human diseases (2007, background): “pression of GRP78 is able to inhibit the activation of SREBPs and the genes under their regulation [113], which implies that GRP78 may be a potential factor to inhibit atherosclerosis.”
• The role for endoplasmic reticulum stress in diabetes mellitus. (2008, background): “steatosis (268), whereas BiP overexpression inhibits SREBP”
• Endoplasmic Reticulum Stress in Liver Disease (2010, background): “Elevated homocysteine levels induce ER stress in many cell types, including hepatocytes and vascular endothelial cell [145,160].”
• Endoplasmic Reticulum Stress and Associated ROS (2016, background): “Accumulation of homocysteine is considered to be a risk factor, produced as a result of ER stress with increased expression of BiP/Grp78, Grp94, CHOP, Herp, and regulation of T-cell death-associated gene 51 (TDAG51) [134–136].”
• Emerging risk factors for atherosclerotic vascular disease: a critical review of the evidence. (2003, background): “proliferation, and endoplasmic reticulum stress.(86,87,93) A common gene mutation encoding”