ArticleThe American journal of pathology1997
The potential role of BAX and BCL-2 expression in diffuse alveolar damage.
Article in The American journal of pathology, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 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
36 citing papers in PubMed, 106 citations in OpenAlex.
- Longitudinally cultured precision cut lung slices as a predictiveNanomedicine (London, England) · 2026Article
- Proteomic Analysis of TCGA Data Reveals Limited Prognostic Value of p53 but Suggests BAX as a Potential Survival Marker in Cervical Carcinoma.International journal of molecular sciences · 2026Article
- How cells die determines the consequences of tissue repair: roles of programmed cell death in lung injury on the progression of pulmonary fibrosis.Molecular and cellular biochemistry · 2026Review
- MDM2 Is Essential to Maintain the Homeostasis of Epithelial Cells by Targeting p53.Journal of innate immunity · 2024Article
- Topical Administration of an Apoptosis Inducer Mitigates Bleomycin-Induced Skin Fibrosis.ACS pharmacology & translational science · 2023Article
- Inhibition of gp130 alleviates LPS-induced lung injury by attenuating apoptosis and inflammation through JAK1/STAT3 signaling pathway.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023Article
- Stratifin as a novel diagnostic biomarker in serum for diffuse alveolar damage.Nature communications · 2022Article
- Serum stratifin and presepsin as candidate biomarkers for early detection of COVID-19 disease progression.Journal of pharmacological sciences · 2022Article
- Blockade of caspase cascade overcomes malaria-associated acute respiratory distress syndrome in mice.Cell death & disease · 2022Article
- Strategies to Overcome Biological Barriers Associated with Pulmonary Drug Delivery.Pharmaceutics · 2022Review
- Influenza A virus NS1 protein represses antiviral immune response by hijacking NF-κB to mediate transcription of type III IFN.Frontiers in cellular and infection microbiology · 2022Article
- Article
- Knockdown of lncRNA MALAT1 Alleviates LPS-Induced Acute Lung Injury via Inhibiting Apoptosis Through the miR-194-5p/FOXP2 Axis.Frontiers in cell and developmental biology · 2020Article
- Neutrophils in the initiation and resolution of acute pulmonary inflammation: understanding biological function and therapeutic potential.The Journal of pathology · 2019Review
- Review
- Digital gene expression analysis in mice lung with coinfection of influenza and streptococcus pneumoniae.Oncotarget · 2017Article
- ResolvinD1 reduces apoptosis and inflammation in primary human alveolar epithelial type 2 cells.Laboratory investigation; a journal of technical methods and pathology · 2016Article
- Intersectin-1s: an important regulator of cellular and molecular pathways in lung injury.Pulmonary circulation · 2013Article
- TLR signaling prevents hyperoxia-induced lung injury by protecting the alveolar epithelium from oxidant-mediated death.Journal of immunology (Baltimore, Md. : 1950) · 2012Article
- Epithelial cell death is an important contributor to oxidant-mediated acute lung injury.American journal of respiratory and critical care medicine · 2011Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Apoptosis of type II pneumocytes has been identified in diffuse alveolar damage (DAD), is associated with p53 and WAF1 expression, and may be of pathogenetic importance. BAX, a homologue of BCL-2, is induced by p53 and is a promoter of apoptosis. The proapoptotic effect of BAX is negatively regulated by its binding with BCL-2. In this study, we sought to investigate that role of BAX and BCL-2 in DAD. We hypothesized that alterations in BAX and BCL-2 expression may be important in determining the susceptibility of type II pneumocytes and interstitial cells to apoptosis. Twenty-eight cases of DAD and 16 control cases (i.e., lung tissues adjacent to resected tumors) were retrieved from the files of the University of Utah and the Armed Forces Institute of Pathology. Immunohistochemical stains were performed with antigen retrieval by microwave using antibodies recognizing BAX and BCL-2. The percentage of positively staining pneumocytes and interstitial cells was estimated in each case to the nearest 10%. BAX expression was markedly increased in pneumocytes and interstitial cells in DAD compared with control lung tissues. In DAD, BAX was identified on an average of 80% of alveolar pneumocytes (range 30 to 100%) and 70% of interstitial cells (range 20 to 90%). In control lungs, BAX was identified on an average of 10% of pneumocytes (range 0 to 20%) but not in interstitial cells. Focal BCL-2 staining was identified in interstitial myofibroblasts in 7 of 25 cases of DAD but was only identified in bronchiolar epithelium of control lungs. These results suggest that the induction of BAX in DAD may enhance the susceptibility of alveolar epithelial cells to apoptosis, whereas BCL-2 expression may contribute to the absence of apoptosis in interstitial myofibroblasts. Expression of BCL-2 in interstitial myofibroblasts may contribute to the development of pulmonary fibrosis in some patients.
Indexed as
Identifiers
9327733PMC1858036W27827702What 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.