ReviewCurrent atherosclerosis reports2012
Endoplasmic reticulum stress in cardiometabolic disorders.
Review in Current atherosclerosis reports, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed, 11 citations in OpenAlex.
- CircSSR1 regulates pyroptosis of pulmonary artery smooth muscle cells through parental protein SSR1 mediating endoplasmic reticulum stress.Respiratory research · 2024Article
- Tumor cell death mediated by peptides that recognize branched intermediates of DNA replication and repair.PloS one · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
When endoplasmic reticulum (ER) homeostasis is disrupted, an adaptive signaling pathway, called the unfolded protein response (UPR) is activated to help ER cope with the stress. The UPR is an important signal transduction pathway, crucial for the survival and function of all cells. Recently, there has been a substantial progress made in understanding the molecular mechanisms of physiological UPR regulation and its role in the pathogenesis of many diseases including metabolic diseases. Studies using mouse models lacking or overexpressing the factors involved in ER stress signaling as well as work performed on humans have revealed the contribution of UPR to disease progression. This review focuses on the regulation of UPR signaling and its relevance in pathogenesis of metabolic diseases.
Indexed as
Identifiers
What OpenQuestion holds
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.