ReviewFree radical biology & medicine2007
Heat shock response and acute lung injury.
Review in Free radical biology & medicine, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 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
52 citing papers in PubMed, 95 citations in OpenAlex.
- Role of biomarkers in pediatric sepsis: What evidence says?World journal of clinical pediatrics · 2026Review
- Gut microbiota modulation in the prevention and treatment of heat stroke.Frontiers in immunology · 2026Review
- Ramping up the Heat: Induction of Systemic and Pulmonary Immune Responses and Metabolic Adaptations in Mice.bioRxiv : the preprint server for biology · 2025Article
- Impact of Heat on Respiratory Hospitalizations among Older Adults in 120 Large U.S. Urban Areas.Annals of the American Thoracic Society · 2025Article
- Combination of HSP90 Inhibitors and HSP70 Inducers Prevent Hydrochloric Acid-Induced Pulmonary Fibrosis in Rabbits.International journal of molecular sciences · 2025Article
- Heat shock protein 27 in the pathogenesis of COVID-19 and non-COVID acute respiratory distress syndrome.Cell stress & chaperones · 2023Observational
- Altered Lung Heat Shock Protein-70 Expression and Severity of Sepsis-Induced Acute Lung Injury in a Chronic Kidney Disease Rat Model.International journal of molecular sciences · 2023Article
- The Link Between Heat Shock Proteins, Renin-Angiotensin System, and the Coagulation Cascade in the Pathogenesis of the Coronavirus-19 Disease.Advances in experimental medicine and biology · 2023Article
- Heat shock protein 70 protects the lungs from hyperoxic injury in a neonatal rat model of bronchopulmonary dysplasia.PloS one · 2023Article
- Macrophage-Targeted Nanomedicines for ARDS/ALI: Promise and Potential.Inflammation · 2022Review
- Effect of elevated temperature on SARS-CoV-2 viability.F1000Research · 2022Article
- TLR4 is required for macrophage efferocytosis during resolution of ventilator-induced lung injury.American journal of physiology. Lung cellular and molecular physiology · 2021Article
- Moderate Fever Cycles as a Potential Mechanism to Protect the Respiratory System in COVID-19 Patients.Frontiers in medicine · 2020Review
- HSF1 Attenuates LPS-Induced Acute Lung Injury in Mice by Suppressing Macrophage Infiltration.Oxidative medicine and cellular longevity · 2020Article
- Possible Modulatory Effect of Tamarind Seed Coat Extract on Fluoride-Induced Pulmonary Inflammation and Fibrosis in Rats.Inflammation · 2018Article
- Observational
- Short-Term Heat Shock Affects Host-Virus Interaction in Mice Infected with Highly Pathogenic Avian Influenza Virus H5N1.Frontiers in microbiology · 2016Article
- Fluoro-edenite and carbon nanotubes: The health impact of 'asbestos-like' fibres.Experimental and therapeutic medicine · 2016Article
- Low dose Hsp90 inhibitor 17AAG protects neural progenitor cells from ischemia induced death.Journal of cell communication and signaling · 2014Article
- The protective effects of glutamine in a rat model of ventilator-induced lung injury.Journal of thoracic disease · 2014Article
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 at 2 institutions in 1 country.
Funding
Abstract
All cells respond to stress through the activation of primitive, evolutionarily conserved genetic programs that maintain homeostasis and assure cell survival. Stress adaptation, which is known in the literature by a myriad of terms, including tolerance, desensitization, conditioning, and reprogramming, is a common paradigm found throughout nature, in which a primary exposure of a cell or organism to a stressful stimulus (e.g., heat) results in an adaptive response by which a second exposure to the same stimulus produces a minimal response. More interesting is the phenomenon of cross-tolerance, by which a primary exposure to a stressful stimulus results in an adaptive response whereby the cell or organism is resistant to a subsequent stress that is different from the initial stress (i.e., exposure to heat stress leading to resistance to oxidant stress). The heat shock response is one of the more commonly described examples of stress adaptation and is characterized by the rapid expression of a unique group of proteins collectively known as heat shock proteins (also commonly referred to as stress proteins). The expression of heat shock proteins is well described in both whole lungs and in specific lung cells from a variety of species and in response to a variety of stressors. More importantly, in vitro data, as well as data from various animal models of acute lung injury, demonstrate that heat shock proteins, especially Hsp27, Hsp32, Hsp60, and Hsp70 have an important cytoprotective role during lung inflammation and injury.
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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.