ArticleThe Journal of clinical investigation1994
Activation of heat-shock transcription factor by graded reductions in renal ATP, in vivo, in the rat.
Article in The Journal of clinical investigation, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 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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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
12 citing papers in PubMed, 68 citations in OpenAlex.
- Relationship of Muscle Apolipoprotein E Expression with Markers of Cellular Stress, Metabolism, and Blood Biomarkers in Cognitively Healthy and Impaired Older Adults.Journal of Alzheimer's disease : JAD · 2023Article
- Heat shock proteins in the kidney.Pediatric nephrology (Berlin, Germany) · 2016Review
- Mice with an absent stress response are protected against ischemic renal injury.Kidney international · 2014Article
- Chromosome substitution modulates resistance to ischemia reperfusion injury in Brown Norway rats.Kidney international · 2013Article
- Increased immunogenicity is an integral part of the heat shock response following renal ischemia.Cell stress & chaperones · 2012Article
- Small interfering RNA mediated Poly (ADP-ribose) Polymerase-1 inhibition upregulates the heat shock response in a murine fibroblast cell line.Journal of inflammation (London, England) · 2011Article
- HSF1 is essential for the resistance of zebrafish eye and brain tissues to hypoxia/reperfusion injury.PloS one · 2011Article
- Na+/K+ -ATPase stabilization by Hsp70 in the outer stripe of the outer medulla in rats during recovery from a low-protein diet.Cell stress & chaperones · 2008Article
- Heat-shock protein 70: molecular supertool?Pediatric nephrology (Berlin, Germany) · 2005Review
- Heat shock factor-1 protein in heat shock factor-1 gene-transfected human epidermoid A431 cells requires phosphorylation before inducing heat shock protein-70 production.The Journal of clinical investigation · 1997Article
- Perturbations in maturation of secretory proteins and their association with endoplasmic reticulum chaperones in a cell culture model for epithelial ischemia.Proceedings of the National Academy of Sciences of the United States of America · 1996Article
- Immediate-early gene induction and MAP kinase activation during recovery from metabolic inhibition in cultured cardiac myocytes.The Journal of clinical investigation · 1995Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Renal ischemia results in both a profound fall in cellular ATP and a rapid induction of the 70 kD heat-shock protein family, HSP-70. The present studies examined the relationship between cellular ATP and induction of the stress response in renal cortex. Cellular ATP, continuously monitored by in vivo 31P-NMR spectroscopy, was reduced and maintained at specific, stable levels in renal cortex by partial aortic occlusion for 45 min. Activation of heat-shock transcription factor (HSF) was detected by gel retardation assay and transcription was confirmed by Northern analysis. Activation of HSF was not present, and HSP-70 mRNA induction did not occur when ATP levels were maintained above 60% preocclusion (control) levels. Reduction in cortical ATP levels to 35-50% preocclusion values resulted in HSF activation and low-level expression of inducible HSP-70 mRNA. Cellular ATP of 20-25% control values resulted in a greater level of HSF activation and subsequent HSP-70 mRNA elaboration. HSF was activated at the end of 15 min of total occlusion. The studies indicate that a 50% reduction in cellular ATP in the renal cortex must occur before the stress response is detectable, that reduction of ATP below 25% control levels produces a more vigorous response, and that reperfusion is not required for initiation of a heat-shock response in the kidney. Cellular ATP, or the metabolic consequences associated with ATP depletion, may be a threshold factor for initiation of a stress response in the kidney.
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Registered trials
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