ArticleOxidative medicine and cellular longevity2019
Toxic Acetaminophen Exposure Induces Distal Lung ER Stress, Proinflammatory Signaling, and Emphysematous Changes in the Adult Murine Lung.
Article in Oxidative medicine and cellular longevity, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 18 citations in OpenAlex.
- Does use of acetaminophen and/or NSAIDs increase the risk of developing bronchopulmonary dysplasia?Pediatric research · 2026Article
- TLR9-mediated innate immune signaling contributes to acetaminophen-induced injury in the developing lung.American journal of physiology. Lung cellular and molecular physiology · 2026Article
- Antimicrobial potentials and challenges of paracetamol: A comprehensive reassessment based on database reports.Pharmaceutical science advances · 2025Review
- Effects of a novel acetaminophen analog on cardiorespiratory compensatory responses and survival in a male rat model of traumatic hemorrhage.Physiological reports · 2025Article
- Developmentally Regulated CYP2E1 Expression Is Associated with a Fetal Pulmonary Transcriptional Response to Maternal Acetaminophen Exposure.Biomedicines · 2025Article
- A Single Early-Life Acetaminophen Exposure Causes Persistent Abnormalities in the Murine Lung.American journal of respiratory cell and molecular biology · 2025Article
- Absence of IκBβ/NFκB signaling does not attenuate acetaminophen-induced hepatic injury.Anatomical record (Hoboken, N.J. : 2007) · 2025Article
- Predicting the prognosis in patients with sepsis by an endoplasmic reticulum stress gene signature.Aging · 2023Article
- Acetaminophen for the patent ductus arteriosus: has safety been adequately demonstrated?Journal of perinatology : official journal of the California Perinatal Association · 2023Review
- Racing against time: leveraging preclinical models to understand pulmonary susceptibility to perinatal acetaminophen exposures.American journal of physiology. Lung cellular and molecular physiology · 2022Review
- APAP-Induced IκBβ/NFκB Signaling Drives Hepatic Il6 Expression and Associated Sinusoidal Dilation.Toxicological sciences : an official journal of the Society of Toxicology · 2022Article
- Pulmonary implications of acetaminophen exposures independent of hepatic toxicity.American journal of physiology. Lung cellular and molecular physiology · 2021Article
- The developing murine lung is susceptible to acetaminophen toxicity.American journal of physiology. Lung cellular and molecular physiology · 2021Article
- Novel Insight into the Role of Endoplasmic Reticulum Stress in the Pathogenesis of Myocardial Ischemia-Reperfusion Injury.Oxidative medicine and cellular longevity · 2021Review
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
Abstract
Clinical studies have demonstrated a strong association between both acute toxic exposure and the repetitive, chronic exposure to acetaminophen (APAP) with pulmonary dysfunction. However, the mechanisms underlying this association are unknown. Preclinical reports have demonstrated that significant bronchiolar injury occurs with toxic APAP exposure, but very little information exists on how the distal lung is affected. However, cells in the alveolar space, including the pulmonary epithelium and resident macrophages, express the APAP-metabolizing enzyme CYP2E1 and are a potential source of toxic metabolites and subsequent distal lung injury. Thus, we hypothesized that distal lung injury would occur in a murine model of toxic APAP exposure. Following exposure of APAP (280 mg/kg, IP), adult male mice were found to have significant proximal lung histopathology as well as distal lung inflammation and emphysematous changes. Toxic APAP exposure was associated with increased CYP2E1 expression in the distal lung and accumulation of APAP-protein adducts. This injury was associated with distal lung activation of oxidant stress, endoplasmic reticulum stress, and inflammatory stress response pathways. Our findings confirm that following toxic APAP exposure, distal lung CYP2E1 expression is associated with APAP metabolism, tissue injury, and oxidant, inflammatory, and endoplasmic reticulum signaling. This previously unrecognized injury may help improve our understanding of the relationship between APAP and pulmonary-related morbidity.
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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.