ArticleEnvironmental health perspectives1990
Responses of the lung to toxic injury.
Article in Environmental health perspectives, 1990. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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
6 citing papers in PubMed, 49 citations in OpenAlex.
- Targeting ATP12A, a Nongastric Proton Pump α Subunit, for Idiopathic Pulmonary Fibrosis Treatment.American journal of respiratory cell and molecular biology · 2023Article
- TGF beta inhibits HGF, FGF7, and FGF10 expression in normal and IPF lung fibroblasts.Physiological reports · 2018Article
- TGF beta inhibits expression of SP-A, SP-B, SP-C, but not SP-D in human alveolar type II cells.Biochemical and biophysical research communications · 2018Article
- Keeping it together: Pulmonary alveoli are maintained by a hierarchy of cellular programs.BioEssays : news and reviews in molecular, cellular and developmental biology · 2015Review
- The Witschi Hypothesis revisited after 35 years: genetic proof from SP-C BRICHOS domain mutations.American journal of physiology. Lung cellular and molecular physiology · 2013Review
- Immuno- and lectin histochemistry of epithelial subtypes and their changes in a radiation-induced lung fibrosis model of the mini pig.Histochemistry · 1993Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Analysis of toxic lung damage may focus on the offending agent and define patterns of bioactivation and interactions with the target tissues. It may also focus on a study of the biological response. While it was originally thought that cell proliferation, particularly Type II epithelial cell proliferation following lung injury, was a common event, it now has become obvious that on occasion proliferation occurs only late after the initial lung damage. Also Type II cell proliferation can occur in the absence of alveolar Type I cell damage. Delayed reepithelialization of the alveolar surface may lead to pulmonary fibrosis. Toxicological interactions often can be best recognized and defined by the extensive lesions that result from concomitant or sequential exposure to such toxic agents as ozone and acidic aerosols or anticancer drugs and oxygen. A correlation of cell proliferation and tumor development in mouse lung has shown that target cell hyperplasia is not a necessary prerequisite for enhanced tumor development. On the other hand, oxygen-induced proliferation of the neuroendocrine cell population results in the short-term development of neuroendocrine lung cell cancer in hamsters. While it is possible to draw some conclusions from an analysis of the lung response to toxic injury, predictions made from such knowledge are sometimes, but not necessarily always, correct.
Indexed as
Identifiers
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.