ReviewNature reviews. Cardiology2021
Endoplasmic reticulum stress and unfolded protein response in cardiovascular diseases.
Review in Nature reviews. Cardiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 386 papers, 1 of them a synthesis that pooled it.
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
386 citing papers in PubMed, 1 synthesis or guideline pooled it, 681 citations in OpenAlex.
- Resistance Exercise Training Mitigates Cardiac Remodeling Induced by a High-Fat Diet in Rodents: A Systematic Review.Arquivos brasileiros de cardiologia · 2024Pooled it
- Acupuncture suppresses the endoplasmic reticulum stress-c-Jun N-terminal kinase pathway to inhibit chondrocyte apoptosis and attenuate knee osteoarthritis.Cell stress & chaperones · 2026Article
- Atherosclerotic Cell Fates: A Single-Cell View of ER Stress.Journal of cardiovascular development and disease · 2026Review
- ANGII Initiated HSF2 Trans-Activating HIF-1α Through Induction of ER Stress to Promote Cardiac Hypertrophy.Clinical and experimental pharmacology & physiology · 2026Article
- Endoplasmic reticulum stress exacerbates ischemia-reperfusion-induced pulmonary endothelial barrier dysfunction by activating TXNDC5.Journal of advanced research · 2026Article
- THSD7A Exacerbates Atherosclerosis via Activation of Signaling Axis αvβ3/CEBPD/IL1A.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Hypertensive mt. tRNARedox biology · 2026Article
- Endoplasmic reticulum stress is associated with cardiac effects of bisphenol S independently of a high-fat diet.Histochemistry and cell biology · 2026Article
- A Novel Pak1 Activator Ameliorates ER Stress for HFpEF Therapy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Targeting eHsp90α/GRP78 signaling-mediated endothelial barrier dysfunction in diabetic atherosclerosis: evidence from clinical and experimental studies.Molecular and cellular biochemistry · 2026Article
- Mitochondria‑endoplasmic reticulum contact site nexus: Molecular integration, disease pathogenesis and therapeutic opportunities (Review).International journal of molecular medicine · 2026Review
- Review
- [Protective effect of the endoplasmic reticulum stress inhibitor 4-phenylbutyric acid against myocardial injury in septic mice].Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2026Article
- Review
- Article
- Enzyme-Inspired Design of Redox-Active Molecules for Promotion of Oxidative Protein Folding.Chembiochem : a European journal of chemical biology · 2026Review
- HIF1α Attenuates Doxorubicin-Induced Cardiotoxicity by Activating TEX264-Associated ER-phagy.Journal of the American Heart Association · 2026Article
- ORMDL3 as Key Regulator of Endothelial Dysfunction in Atherosclerosis via Sphingolipid Biosynthesis.Inflammation · 2026Article
- Lycopene Attenuates Hexavalent Chromium-Induced Hepatotoxicity in Mice by Modulating the Nrf2 Signaling Pathway and the Unfolded Protein Response.Biological trace element research · 2026Article
- Molecular damage associated with ageing drives inflammation in cardiovascular disease.Nature reviews. Cardiology · 2026Review
326 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
5 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cardiovascular diseases (CVDs), such as ischaemic heart disease, cardiomyopathy, atherosclerosis, hypertension, stroke and heart failure, are among the leading causes of morbidity and mortality worldwide. Although specific CVDs and the associated cardiometabolic abnormalities have distinct pathophysiological and clinical manifestations, they often share common traits, including disruption of proteostasis resulting in accumulation of unfolded or misfolded proteins in the endoplasmic reticulum (ER). ER proteostasis is governed by the unfolded protein response (UPR), a signalling pathway that adjusts the protein-folding capacity of the cell to sustain the cell's secretory function. When the adaptive UPR fails to preserve ER homeostasis, a maladaptive or terminal UPR is engaged, leading to the disruption of ER integrity and to apoptosis. ER stress functions as a double-edged sword, with long-term ER stress resulting in cellular defects causing disturbed cardiovascular function. In this Review, we discuss the distinct roles of the UPR and ER stress response as both causes and consequences of CVD. We also summarize the latest advances in our understanding of the importance of the UPR and ER stress in the pathogenesis of CVD and discuss potential therapeutic strategies aimed at restoring ER proteostasis in CVDs.
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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.