ArticleCell stress & chaperones2015
Celastrol, an oral heat shock activator, ameliorates multiple animal disease models of cell death.
Article in Cell stress & chaperones, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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
17 citing papers in PubMed, 30 citations in OpenAlex.
- Celastrol Attenuates Doxorubicin-Induced Heart Failure by Preserving Mitochondrial Integrity and Suppressing Oxidative Stress and Is Accompanied by Changes in Gut Microbiota.Pharmaceuticals (Basel, Switzerland) · 2026Article
- In Silico Perturbation Identifies Transcription Factors as Protective Targets in HSPCs After Irradiation.International journal of molecular sciences · 2026Article
- Review
- Celastrol: A Promising Agent Fighting against Cardiovascular Diseases.Antioxidants (Basel, Switzerland) · 2022Review
- Neuroprotective Effects of Celastrol in Neurodegenerative Diseases-Unscramble Its Major Mechanisms of Action and Targets.Aging and disease · 2022Review
- Inhibition of mitochondrial respiration has fundamentally different effects on proliferation, cell survival and stress response in immature versus differentiated cardiomyocyte cell lines.Frontiers in cell and developmental biology · 2022Article
- Ferroptosis inducer erastin sensitizes NSCLC cells to celastrol through activation of the ROS-mitochondrial fission-mitophagy axis.Molecular oncology · 2021Article
- The mechanisms of celastrol in treating papillary thyroid carcinoma based on network pharmacology and experiment verification.Annals of translational medicine · 2021Article
- Heat shock protein 90 inhibition and multi-target approach to maximize cardioprotection in ischaemic injury.British journal of pharmacology · 2020Review
- Effects of diclofenac on the pharmacokinetics of celastrol in rats and its transport.Pharmaceutical biology · 2018Article
- Protective effect of celastrol on myocardial ischemia-reperfusion injury.Anatolian journal of cardiology · 2017Article
- Article
- The heat shock response in neurons and astroglia and its role in neurodegenerative diseases.Molecular neurodegeneration · 2017Review
- Chaperone co-inducer BGP-15 inhibits histone deacetylases and enhances the heat shock response through increased chromatin accessibility.Cell stress & chaperones · 2017Article
- Protein Quality Control and the Amyotrophic Lateral Sclerosis/Frontotemporal Dementia Continuum.Frontiers in molecular neuroscience · 2017Article
- The central role of heat shock factor 1 in synaptic fidelity and memory consolidation.Cell stress & chaperones · 2016Article
- Induction of heat shock proteins in differentiated human neuronal cells following co-application of celastrol and arimoclomol.Cell stress & chaperones · 2016Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
Abstract
Protein homeostatic regulators have been shown to ameliorate single, loss-of-function protein diseases but not to treat broader animal disease models that may involve cell death. Diseases often trigger protein homeostatic instability that disrupts the delicate balance of normal cellular viability. Furthermore, protein homeostatic regulators have been delivered invasively and not with simple oral administration. Here, we report the potent homeostatic abilities of celastrol to promote cell survival, decrease inflammation, and maintain cellular homeostasis in three different disease models of apoptosis and inflammation involving hepatocytes and cardiomyocytes. We show that celastrol significantly recovers the left ventricular function and myocardial remodeling following models of acute myocardial infarction and doxorubicin-induced cardiomyopathy by diminishing infarct size, apoptosis, and inflammation. Celastrol prevents acute liver dysfunction and promotes hepatocyte survival after toxic doses of thioacetamide. Finally, we show that heat shock response (HSR) is necessary and sufficient for the recovery abilities of celastrol. Our observations may have dramatic clinical implications to ameliorate entire disease processes even after cellular injury initiation by using an orally delivered HSR activator.
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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.