ReviewRedox biology2020
Insights of heat shock protein 22 in the cardiac protection against ischemic oxidative stress.
Review in Redox biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.
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
18 citing papers in PubMed, 1 synthesis or guideline pooled it, 28 citations in OpenAlex.
- The Heart of the Alzheimer's: A Mindful View of Heart Disease.Frontiers in physiology · 2020Pooled it
- Recognition and confirmation of key genes associated with nicotinamide metabolism in acute myocardial infarction.Hereditas · 2026Article
- STAT-Mediated Mitochondrial Regulation in Cardiovascular Diseases: Mechanistic Insights and STAT3-Focused Therapeutic Strategies.Biomolecules · 2026Review
- Cardiomyocyte programmed cell death in dilated cardiomyopathy: molecular crosstalk and therapeutic implications.Frontiers in cell and developmental biology · 2026Review
- Involvement of Oxidative Stress and Antioxidants in Modification of Cardiac Dysfunction Due to Ischemia-Reperfusion Injury.Antioxidants (Basel, Switzerland) · 2025Review
- Heat shock protein 22 alleviates doxorubicin-induced kidney injury by suppressing oxidative stress and apoptosis.Scientific reports · 2024Article
- The ischemia-enhanced myocardial infarction protection-related lncRNA protects against acute myocardial infarction.MedComm · 2024Article
- Heat Shock Protein 22 Attenuates Nerve Injury-induced Neuropathic Pain Via Improving Mitochondrial Biogenesis and Reducing Oxidative Stress Mediated By Spinal AMPK/PGC-1α Pathway in Male Rats.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2024Article
- Homo-oxidized HSPB1 protects H9c2 cells against oxidative stress via activation of KEAP1/NRF2 signaling pathway.iScience · 2023Article
- Evaluation of Vasodilatory Effect of Nitroglycerin in Cardioplegia Solution on Patients Undergoing Coronary Artery Bypass Graft Surgery.ARYA atherosclerosis · 2023Article
- Macrophage-specific autophagy-related gene HSPB8 is involved in the macrophage polarization in atherosclerosis.BMC cardiovascular disorders · 2023Article
- Furosemide-induced systemic dehydration alters the proteome of rabbit vocal folds.Journal of proteomics · 2022Article
- Role of the mtDNA Mutations and Mitophagy in Inflammaging.International journal of molecular sciences · 2022Review
- HSPB8 Overexpression Ameliorates Cognitive Impairment in Diabetic Mice via Inhibiting NLRP3 Inflammation Activation.Oxidative medicine and cellular longevity · 2022Article
- Heat Shock Protein 22 in Physiological and Pathological Hearts: Small Molecule, Large Potentials.Cells · 2021Review
- Hsp22 ameliorates lipopolysaccharide-induced myocardial injury by inhibiting inflammation, oxidative stress, and apoptosis.Bioengineered · 2021Article
- Hsp22 Deficiency Induces Age-Dependent Cardiac Dilation and Dysfunction by Impairing Autophagy, Metabolism, and Oxidative Response.Antioxidants (Basel, Switzerland) · 2021Article
- Heat Shock Proteins in Oxidative Stress and Ischemia/Reperfusion Injury and Benefits from Physical Exercises: A Review to the Current Knowledge.Oxidative medicine and cellular longevity · 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
4 authors at 2 institutions in 2 countries.
Funding
Abstract
the acute and chronic myocardial ischemia results in oxidative stress that impairs myocardial contractility and eventually leads to heart failure. However, the underlying regulatory molecular mechanisms are not fully understood. The heat shock protein 22 (Hsp22), a small-molecular-weight protein preferentially expressed in the heart, was found to be dramatically increased in the cardiac oxidative stress conditions in both human and animal models after the acute and chronic ischemia. Overexpression of Hsp22 largely protects the heart against ischemic damage. Mechanistically, overexpression of Hsp22 attenuates hypoxia-induced oxidative phosphorylation in mitochondrial and the high rate of superoxide production. Short term gene delivery of Hsp22 reduces the infarct size caused by the ischemia/reperfusion, providing a clinical therapeutic potential. This review discusses the new progress of the studies on Hsp22 by focusing on its protective effect against the excessive cardiac oxidative stress, including its adaptive induction in myocardium upon the oxidative stress, its protective role in myocardial ischemia/reperfusion, its regulation in mitochondrial oxidative phosphorylation and the underlying molecular signaling pathways promoting cell survival. This information will increase our understanding of the molecular regulation of cardiac adaption under the oxidative stress and the potential therapeutic relevance.
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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.