ReviewBritish journal of pharmacology2018
Endoplasmic reticulum stress in the heart: insights into mechanisms and drug targets.
Review in British journal of pharmacology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 120 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
120 citing papers in PubMed.
- Beyond the Pump: Unravelling Immunometabolic Crosstalk and Organelle Dynamics in Sepsis-Induced Cardiomyopathy.Journal of cardiovascular translational research · 2026Article
- Endoplasmic reticulum stress is associated with cardiac effects of bisphenol S independently of a high-fat diet.Histochemistry and cell biology · 2026Article
- Review
- Programmed Cell Death of Endothelial Cells in Ischemic Heart Disease: Mechanism and Potential Cell and Gene Therapeutic Prospects.Bioengineering (Basel, Switzerland) · 2026Review
- The complex link of the folate-homocysteine axis to myocardial hypertrophy and heart failure: from mechanistic exploration to clinical vision.Journal of advanced research · 2026Review
- Organelle homeostasis disruption: A driving force in the progression of cardiomyopathy (Review).Experimental and therapeutic medicine · 2026Review
- SGPP2 Ameliorates Chronic Heart Failure by Attenuating ERS via the SIRT1/AMPK Pathway.Current issues in molecular biology · 2026Article
- Targeting the cardio-neuro axis through nutrition: inflammatory mechanisms linking cardiovascular and neurodegenerative diseases.Frontiers in nutrition · 2026Article
- Ursodeoxycholic acid as a potential cardioprotective agent: molecular mechanisms, experimental evidence, and clinical perspectives.Frontiers in pharmacology · 2026Review
- Unravelling the Pathogenesis of Heart Failure with Preserved Ejection Fraction: The Pivotal Role of Autophagy and Endoplasmic Reticulum Stress.European cardiology · 2026Review
- Article
- ER stress inhibitor 4PBA attenuates hindlimb unloading-induced cardiac mitochondrial and metabolic dysfunction.Pflugers Archiv : European journal of physiology · 2025Article
- Magnesium-assisted hydrogen improves isoproterenol-induced heart failure.Medical gas research · 2025Article
- Pimobendan alleviates myocyte apoptosis and fibrosis associated with mitral regurgitation by targeting endoplasmic reticulum stress.Animal models and experimental medicine · 2025Article
- Cellular and Molecular Pathways in Diabetes-Associated Heart Failure: Emerging Mechanistic Insights and Therapeutic Opportunities.Current issues in molecular biology · 2025Review
- Review
- Article
- Dietary influences on chemotherapy sensitivity and cardiotoxicity modulated by IRE1 targeting in triple-negative breast cancer in female mice.Physiological reports · 2025Article
- Novel insights into beta cell ER stress CHOP and its role in HFpEF development.Cardiovascular diabetology · 2025Article
- Altered protein homeostasis in cardiovascular diseases contributes to Alzheimer's-like neuropathology.Basic research in cardiology · 2025Article
60 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
Abstract
The endoplasmic reticulum (ER) serves several essential cellular functions including protein synthesis, protein folding, protein translocation, calcium homoeostasis and lipid biosynthesis. Physiological or pathological stimuli, which disrupt ER homoeostasis and disturb its functions, lead to an accumulation of misfolded and unfolded proteins, a condition referred to as ER stress. ER stress triggers the unfolded protein response to restore the homoeostasis of ER, through activating transcriptional and translational pathways. However, prolonged ER stress will lead to cell dysfunction and apoptosis. Recent evidence revealed that ER stress is involved in the development and progression of various heart diseases, such as cardiac hypertrophy, ischaemic heart diseases and heart failure. Therefore, improved understanding of the molecular mechanisms of ER stress in heart disease will help to investigate more potential targets for new therapeutic interventions and drug discovery. LINKED ARTICLES: This article is part of a themed section on Spotlight on Small Molecules in Cardiovascular Diseases. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v175.8/issuetoc.
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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.