ReviewJournal of molecular and cellular cardiology2018
The unfolded protein response in ischemic heart disease.
Review in Journal of molecular and cellular cardiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
What it found
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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.
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Who cites it
43 citing papers in PubMed, 79 citations in OpenAlex.
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- Orf132: a critical gene for LSDV replication and its role in Er stress-related apoptosis.Virology journal · 2025Article
- Therapeutic implications of endoplasmic reticulum stress gene CCL3 in cervical squamous cell carcinoma.Cell biology and toxicology · 2025Article
- Activation of the PERK/MANF/STAT3 Pathway in Astrocytes Promotes Synaptic Remodeling and Neurological Recovery in the Acute Phase After Stroke in Mice.Neural plasticity · 2025Article
- Endoplasmic reticulum stress in cardiomyopathies: from the unfolded protein response to therapeutic opportunities.Frontiers in cardiovascular medicine · 2025Review
- Potential of natural drug modulation of endoplasmic reticulum stress in the treatment of myocardial injury.Journal of pharmaceutical analysis · 2024Review
- Endoplasmic reticulum stress in diseases.MedComm · 2024Review
- Nuclear Factor Erythroid 2-Related Factor 2 is Essential for Low-Normobaric Oxygen Treatment-Mediated Blood-Brain Barrier Protection Following Ischemic Stroke.Molecular neurobiology · 2024Article
- 1,25-dihydroxyvitamin DNutrition research and practice · 2024Article
- A comprehensive analysis of the role of native and modified HDL in ER stress in primary macrophages.Frontiers in cardiovascular medicine · 2024Article
- Puerarin attenuates myocardial ischemic injury and endoplasmic reticulum stress by upregulating the Mzb1 signal pathway.Frontiers in pharmacology · 2024Article
- Oridonin Promotes Apoptosis in Rheumatoid Arthritis Fibroblast-like Synoviocytes Through PERK/eIF2α/CHOP of Endoplasmic Reticulum Stress Pathway.DNA and cell biology · 2023Article
- Finding New Targets for the Treatment of Heart Failure: Endoplasmic Reticulum Stress and Autophagy.Journal of cardiovascular translational research · 2023Review
- Ceapin-A7 potentiates lipopolysaccharide-induced endothelial injury.Journal of biochemical and molecular toxicology · 2023Article
- Emerging roles of the RNA modifications N6-methyladenosine and adenosine-to-inosine in cardiovascular diseases.Molecular therapy. Nucleic acids · 2022Review
- Interplay between ZnInternational journal of molecular sciences · 2022Review
- Naringenin Alleviates Renal Ischemia Reperfusion Injury by Suppressing ER Stress-Induced Pyroptosis and Apoptosis through Activating Nrf2/HO-1 Signaling Pathway.Oxidative medicine and cellular longevity · 2022Article
- An update on the unfolded protein response in brain ischemia: Experimental evidence and therapeutic opportunities.Neurochemistry international · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
Ischemic heart disease is a severe stress condition that causes extensive pathological alterations and triggers cardiac cell death. Accumulating evidence suggests that the unfolded protein response (UPR) is strongly induced by myocardial ischemia. The UPR is an evolutionarily conserved cellular response to cope with protein-folding stress, from yeast to mammals. Endoplasmic reticulum (ER) transmembrane sensors detect the accumulation of unfolded proteins and stimulate a signaling network to accommodate unfolded and misfolded proteins. Distinct mechanisms participate in the activation of three major signal pathways, viz. protein kinase RNA-like ER kinase, inositol-requiring protein 1, and activating transcription factor 6, to transiently suppress protein translation, enhance protein folding capacity of the ER, and augment ER-associated degradation to refold denatured proteins and restore cellular homeostasis. However, if the stress is severe and persistent, the UPR elicits inflammatory and apoptotic pathways to eliminate terminally affected cells. The ER is therefore recognized as a vitally important organelle that determines cell survival or death. Recent studies indicate the UPR plays critical roles in the pathophysiology of ischemic heart disease. The three signaling branches may elicit distinct but overlapping effects in cardiac response to ischemia. Here, we outline the findings and discuss the mechanisms of action and therapeutic potentials of the UPR in the treatment of ischemic heart disease.
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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.