ArticleInternational journal of clinical and experimental medicine2017
Upregulation of autophagy genes and the unfolded protein response in human heart failure.
Article in International journal of clinical and experimental medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 23 citations in OpenAlex.
- Research progress on targeting autophagy pathways with medicinal plants and their active metabolites for the treatment of heart failure.Frontiers in pharmacology · 2026Review
- Article
- [Fuyu Decoction improves ventricular remodeling in rats with heart failure by inhibiting AMPK/mTOR pathway-mediated autophagy].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2023Article
- Dichloroacetate ameliorates myocardial ischemia-reperfusion injury via regulating autophagy and glucose homeostasis.Archives of medical science : AMS · 2023Article
- Preventing unfolded protein response-induced ion channel dysregulation to treat arrhythmias.Trends in molecular medicine · 2022Review
- Inhibition of the unfolded protein response reduces arrhythmia risk after myocardial infarction.The Journal of clinical investigation · 2021Article
- Adipocyte-specific deletion of HuR induces spontaneous cardiac hypertrophy and fibrosis.American journal of physiology. Heart and circulatory physiology · 2021Article
- Moxibustion Improves Chronic Heart Failure by Inhibiting Autophagy and Inflammation via Upregulation of mTOR Expression.Evidence-based complementary and alternative medicine : eCAM · 2021Article
- The protective role of the miR-25-mediated notch signaling pathway in the memory capacity and brain tissue of mice with central nervous system infections.American journal of translational research · 2021Article
- Supplemental 25-hydroxycholecalciferol Alleviates Inflammation and Cardiac Fibrosis in Hens.International journal of molecular sciences · 2020Article
- Selective enhancement of cardiomyocyte efficiency results in a pernicious heart condition.PloS one · 2020Article
- Lamin B is a target for selective nuclear PQC by BAG3: implication for nuclear envelopathies.Cell death & disease · 2019Article
- The role of the unfolded protein response in arrhythmias.Channels (Austin, Tex.) · 2018Review
- Stress Coping Strategies in the Heart: An Integrated View.Frontiers in cardiovascular medicine · 2018Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
The cellular environment of the mammalian heart constantly is challenged with environmental and intrinsic pathological insults, which affect the proper folding of proteins in heart failure. The effects of damaged or misfolded proteins on the cell can be profound and result in a process termed "proteotoxicity". While proteotoxicity is best known for its role in mediating the pathogenesis of neurodegenerative diseases such as Alzheimer's disease, its role in human heart failure also has been recognized. The UPR involves three branches, including PERK, ATF6, and IRE1. In the presence of a misfolded protein, the GRP78 molecular chaperone that normally interacts with the receptors PERK, ATF6, and IRE-1 in the endoplasmic reticulum detaches to attempt to stabilize the protein. Mouse models of cardiac hypertrophy, ischemia, and heart failure demonstrate increases in activity of all three branches after removing GRP78 from these internal receptors. Recent studies have linked elevated PERK and CHOP in vitro with regulation of ion channels linked with human systolic heart failure. With this in mind, we specifically investigated ventricular myocardium from 10 patients with a history of conduction system defects or arrhythmias for expression of UPR and autophagy genes compared to myocardium from non-failing controls. We identified elevated
Indexed as
Identifiers
28794819PMC5546743W2612212442What 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.