ReviewBioMed research international2014
Role of endoplasmic reticulum stress in atherosclerosis and diabetic macrovascular complications.
Review in BioMed research international, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
39 citing papers in PubMed.
- Exploring Ceramide C16:0 as a Novel Biomarker and Therapeutic Target for Atherosclerosis.Journal of the American Heart Association · 2026Review
- Biochemical origin of (near-) linear curvature constant (W')-European journal of applied physiology · 2025Article
- IRE1α: from the function to the potential therapeutic target in atherosclerosis.Molecular and cellular biochemistry · 2024Review
- Current views on selenoprotein S in the pathophysiological processes of diabetes-induced atherosclerosis: potential therapeutics and underlying biomarkers.Diabetology & metabolic syndrome · 2024Review
- MicroRNA Regulation for Inflammasomes in High Glucose-Treated ARPE-19 Cells.Journal of ophthalmology · 2024Article
- Diclofenac Diminished the Unfolded Protein Response (UPR) Induced by Tunicamycin in Human Endothelial Cells.Molecules (Basel, Switzerland) · 2022Article
- Role of store-operated Ca2+ entry in cardiovascular disease.Cell communication and signaling : CCS · 2022Review
- Atherosclerosis in HIV Patients: What Do We Know so Far?International journal of molecular sciences · 2022Review
- From Mitochondria to Atherosclerosis: The Inflammation Path.Biomedicines · 2021Review
- Some Molecular and Cellular Stress Mechanisms Associated with Neurodegenerative Diseases and Atherosclerosis.International journal of molecular sciences · 2021Review
- Shared Molecular Mechanisms between Atherosclerosis and Periodontitis by Analyzing the Transcriptomic Alterations of Peripheral Blood Monocytes.Computational and mathematical methods in medicine · 2021Article
- The microscopic anatomy of endothelial cells in human atherosclerosis: Focus on ER and mitochondria.Journal of anatomy · 2020Article
- NOD1 and NOD2 in inflammatory and infectious diseases.Immunological reviews · 2020Review
- NLPR3 Inflammasomes and Their Significance for Atherosclerosis.Biomedicines · 2020Review
- Nucleotide-binding oligomerization domain protein 2 deficiency enhances CHOP expression and plaque necrosis in advanced atherosclerotic lesions.The FEBS journal · 2020Article
- Recent aspects of the effects of zinc on human health.Archives of toxicology · 2020Review
- Nucleotide-binding oligomerization domain protein 2 attenuates ER stress-induced cell death in vascular smooth muscle cells.BMB reports · 2019Article
- Nitric Oxide and Hydrogen Sulfide Regulation of Ischemic Vascular Growth and Remodeling.Comprehensive Physiology · 2019Review
- High glucose causes apoptosis of rabbit corneal epithelial cells involving activation of PERK-eIF2α-CHOP-caspase-12 signaling pathway.International journal of ophthalmology · 2019Article
- Molecular docking studies of salubrinal and its analogs as inhibitors of the GADD34:PP1 enzyme.ADMET & DMPK · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Age-related changes in endoplasmic reticulum (ER) are associated with stress of this cell organelle. Unfolded protein response (UPR) is a normal physiological reaction of a cell in order to prevent accumulation of unfolded and misfolded proteins in the ER and improve the normal ER function. However, in pathologic conditions such as atherosclerosis, obesity, and diabetes, ER function becomes impaired, leading to the development of ER stress. In chronic ER stress, defective posttranslational protein folding results in deposits of aberrantly folded proteins in the ER and the induction of cell apoptosis mediated by UPR sensors C/EBPα-homologous protein (CHOP) and inositol requiring protein-1 (IRE1). Since ER stress and ER-induced cell death play a nonredundant role in the pathogenesis of atherosclerosis and diabetic macrovascular complications, pharmaceutical targeting of ER stress components and pathways may be beneficial in the treatment and prevention of cardiovascular pathology.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.