ArticleThe EMBO journal2002
Mouse heat shock transcription factor 1 deficiency alters cardiac redox homeostasis and increases mitochondrial oxidative damage.
Article in The EMBO journal, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 109 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.
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Who cites it
109 citing papers in PubMed, 239 citations in OpenAlex.
- PROGRESS Study: Longitudinal analysis of antioxidant status and its relationship with heat shock proteins in children with chronic kidney disease.Pediatric nephrology (Berlin, Germany) · 2026Article
- Enhancement of antioxidant function in various organs in mice using combined thermal and radon inhalation treatment.Journal of radiation research · 2026Article
- Review
- Heat shock transcription factors in development and disease.Disease models & mechanisms · 2026Review
- Transcriptional responses to proteotoxic stressors are profoundly diverse and tissue-specific.Cell stress & chaperones · 2026Article
- EP300 confers protection against acute pancreatitis via acetylating HSF1 and promoting PRKN-mediated mitophagy in pancreatic acinar cells.Cell communication and signaling : CCS · 2025Article
- Peripheral blood heat shock protein 27 correlates with information processing speed and executive function, potentially serving as a marker for mild cognitive impairment in patients with type 2 diabetes mellitus.Diabetology & metabolic syndrome · 2025Article
- Hsf1 is essential for proteotoxic stress response in smyd1b-deficient embryos and fish survival under heat shock.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Article
- Therapeutic targets in diabetic peripheral neuropathy: heat shock proteins.Frontiers in endocrinology · 2025Review
- Single-cell multi-modal integrative analyses highlight functional dynamic gene regulatory networks directing human cardiac development.Cell genomics · 2024Article
- Gandouling ameliorates liver injury in Wilson's disease through the inhibition of ferroptosis by regulating the HSF1/HSPB1 pathway.Journal of cellular and molecular medicine · 2024Article
- Revealing the metabolic potential and environmental adaptation of nematophagous fungus,Frontiers in microbiology · 2024Article
- The pentose phosphate pathway in health and disease.Nature metabolism · 2023Review
- Antioxidant Enzyme Activity and Serum HSP70 Concentrations in Relation to Insulin Resistance and Lipid Profile in Lean and Overweight Young Men.Antioxidants (Basel, Switzerland) · 2023Article
- Ferroptosis as a potential new therapeutic target for diabetes and its complications.Endocrine connections · 2023Review
- HSF1 and Its Role in Huntington's Disease Pathology.Advances in experimental medicine and biology · 2023Review
- Potential roles for mitochondria-to-HSF1 signaling in health and disease.Frontiers in molecular biosciences · 2023Review
- HSF1 is a driver of leukemia stem cell self-renewal in acute myeloid leukemia.Nature communications · 2022Article
- Cryptococcal Hsf3 controls intramitochondrial ROS homeostasis by regulating the respiratory process.Nature communications · 2022Article
49 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
In this study, using heat shock factor 1 (Hsf1) knockout mice as a model, we tested the hypothesis that HSF1-dependent regulation of heat shock proteins (Hsps) is required to maintain redox state and attenuate oxidative damage in the normal heart. Here we report that, in mice, HSF1 deficiency reduces cardiac expression of Hsp25, alphaB-crystallin and Hsp70, but not Hsp60 and Hsp90. Consistent with the downregulation of Hsp25, for example, a significantly lower glutathione (GSH)/glutathione disulfate (GSSG) ratio was associated with the decreased activity, but not protein content, of glucose 6-phosphate dehydrogenase. Con sequently, superoxide was generated at a higher rate, and several mitochondrial proteins, including adenine nucleotide translocase 1 (ANT1), were more oxidized by HSF1 deficiency in vivo. Oxidative damage to ANT1 protein, a structural component of the mitochondrial permeability transition pore (MPTP), decreases its catalytic activity and increases MPTP opening, respectively. Taken together, our results indicate for the first time that constitutive expression of HSP chaperones requires HSF1 activity, and that such HSF1-dependent requirements are directly and functionally linked to maintain redox homeostasis and antioxidative defenses at normal (37 degrees C) temperature.
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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.