ReviewDisease models & mechanisms2026
Heat shock transcription factors in development and disease.
Review in Disease models & mechanisms, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed.
- GJB2, a novel transcription target of HSF4, confers tumorigenic and metastatic phenotypes and sustains mitochondrial homeostasis in lung adenocarcinoma via the PI3K/AKT pathway.Cell adhesion & migration · 2026Article
- More than the 'master regulator of cytosolic proteostasis': new roles for HSF1 in promoting tissue health.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
Abstract
The heat shock response is a highly conserved cellular defense mechanism against proteotoxic stress, characterized by the induction of heat shock proteins (HSPs) that function as molecular chaperones to maintain protein homeostasis. Central to this response are the heat shock transcription factors (HSFs), which regulate the expression of HSPs. This Review explores the structural and functional relationships of the mammalian HSF family, including HSF1, HSF2, HSF4 and HSF5. We highlight HSF gene expression and function during organismal development and details of HSFs involvement in neurodegenerative diseases, in which they mitigate/counteract protein aggregation and promote neuronal survival, and in cancer, in which they support tumor growth and metastasis. We also examine the interplay between different HSFs and their context-dependent functions, emphasizing their relevance as potential targets for therapeutic intervention. Understanding the diverse roles of these factors is essential for advancing our knowledge of physiological regulation, and for developing targeted therapies for a broad range of diseases.
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What OpenQuestion holds
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.