ArticleCells2020
Aspirin Enhances the Protection of Hsp90 from Heat-Stressed Injury in Cardiac Microvascular Endothelial Cells Through PI3K-Akt and PKM2 Pathways.
Article in Cells, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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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.
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Who cites it
15 citing papers in PubMed, 28 citations in OpenAlex.
- Linking Heat Stress to Impaired Cardiac Repair: The ER Stress-Angiogenesis Axis as a Critical Barrier.International journal of molecular sciences · 2026Review
- Metabolic Reprogramming and Cell Interaction in Atherosclerosis: From Molecular Mechanisms to Therapeutic Strategies.Journal of cardiovascular development and disease · 2025Review
- Reduced Glutathione Promoted Growth Performance by Improving the Jejunal Barrier, Antioxidant Function, and Altering Proteomics of Weaned Piglets.Antioxidants (Basel, Switzerland) · 2025Article
- Heat shock proteins in hypothermia: a review.Frontiers in molecular biosciences · 2025Review
- SULT2B1: a novel therapeutic target in colorectal cancer via modulation of AKT/PKM2-mediated glycolysis and proliferation.Journal of translational medicine · 2024Article
- Investigation of the Potential Mechanism of Compound Dragon's Blood Capsule against Myocardial Ischemia Based on Network Pharmacology.Combinatorial chemistry & high throughput screening · 2024Article
- Association between aspirin and mortality in critically ill patients with atrial fibrillation: a retrospective cohort study based on mimic-IV database.Frontiers in cardiovascular medicine · 2024Article
- The effect of semen cuscutae flavonoid on Sertoli cells and blood-testis barrier in male infertility: integrating network pharmacology and experimental verification.Pharmaceutical biology · 2023Article
- Atheroprotective Aspects of Heat Shock Proteins.International journal of molecular sciences · 2023Review
- The pathogenesis and therapeutic strategies of heat stroke-induced myocardial injury.Frontiers in pharmacology · 2023Review
- The Association between Gut Microbiome Diversity and Composition and Heat Tolerance in Cattle.Microorganisms · 2022Article
- Heat Shock Protein 90 as Therapeutic Target for CVDs and Heart Ageing.International journal of molecular sciences · 2022Review
- Acetylsalicylic acid and salicylic acid present anticancer properties against melanoma by promoting nitric oxide-dependent endoplasmic reticulum stress and apoptosis.Scientific reports · 2020Article
- Dihydroartemisinin Inhibits the Proliferation of Leukemia Cells K562 by Suppressing PKM2 and GLUT1 Mediated Aerobic Glycolysis.Drug design, development and therapy · 2020Article
- Oxidative Stress in Ischemic Heart Disease.Oxidative medicine and cellular longevity · 2020Review
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Heat stress (HS) often causes sudden death of humans and animals due to heart failure, mainly resulting from the contraction of cardiac microvasculature followed by myocardial ischemia. Cardiac microvascular endothelial cells (CMVECs) play an important role in maintaining vasodilatation. Aspirin (ASA) is well known for its protective abilities of febrile animals. However, there is little knowledge about molecular resistance mechanisms of CMVECs and which role ASA may play in this context. Therefore, we used a heat stress model of rat cardiac microvascular endothelial cell cultures in vitro and investigated the cell injuries and molecular resistance mechanism of CMVECs caused by heat stress, and the effect of aspirin (ASA) on it. HS induced severe pathological damage of CMVECs and cellular oxidative stress and dysfunction of NO release. Hsp90 was proven to be indispensable for resisting HS-injury of CMVECs through PI3K-Akt and PKM2 signaling pathways. Meanwhile, PKM2 functioned in reducing Akt phosphorylation. ASA treatment of CMVECs induced a significant expression of Hsp90, which promoted both Akt and PKM2 signals, which are beneficial for relieving HS damage and maintaining the function of CMVECs. Akt activation also promoted HSF-1 that regulates the expression of Hsp70, which is known to assist Hsp90's molecular chaperone function and when released to the extracellular liquid to protect myocardial cells from HS damage. To the best of our knowledge, this is the first study to show that HS damages CMVECs and the protection mechanism of Hsp90 on it, and that ASA provides a new potential strategy for regulating cardiac microcirculation preventing HS-induced heart failure.
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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.