ArticleInternational journal of chronic obstructive pulmonary disease2018
Endoplasmic reticulum chaperone GRP78 mediates cigarette smoke-induced necroptosis and injury in bronchial epithelium.
Article in International journal of chronic obstructive pulmonary disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 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
13 citing papers in PubMed, 28 citations in OpenAlex.
- Review
- Airway remodeling in chronic obstructive pulmonary disease: characteristics and opportunities.Frontiers in medicine · 2025Review
- PGAM5 Modulates Macrophage Polarization, Aggravating Inflammation in COPD via the NF-κB Pathway.International journal of chronic obstructive pulmonary disease · 2025Article
- Resolution Potential of Necrotic Cell Death Pathways.International journal of molecular sciences · 2022Review
- Role of necroptosis in airflow limitation in chronic obstructive pulmonary disease: focus on small-airway disease and emphysema.Cell death discovery · 2022Review
- Cryptotanshinone alleviates myocardial ischemia and reperfusion injury in rats to mitigate ER stress-dependent apoptosis by modulating the JAK1/STAT3 axis.American journal of translational research · 2022Article
- Dysregulation of the miR-30a/BiP axis by cigarette smoking accelerates oral cancer progression.Cancer cell international · 2021Article
- The potential role of necroptosis in clinical diseases (Review).International journal of molecular medicine · 2021Review
- Necroptosis in Pulmonary Diseases: A New Therapeutic Target.Frontiers in pharmacology · 2021Review
- Estrogen administration reduces the risk of pulmonary arterial hypertension by modulating the miR-133a signaling pathways in rats.Gene therapy · 2020Article
- Necroptosis Mediates Cigarette Smoke-Induced Inflammatory Responses in Macrophages.International journal of chronic obstructive pulmonary disease · 2020Article
- Pathogenesis of chronic obstructive pulmonary disease (COPD) induced by cigarette smoke.Journal of thoracic disease · 2019Review
- Autophagy, selective autophagy, and necroptosis in COPD.International journal of chronic obstructive pulmonary diseaseReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Introduction: Bronchial epithelial cell death and airway inflammation induced by cigarette smoke (CS) have been involved in the pathogenesis of COPD. GRP78, belonging to heat shock protein 70 family, has been implicated in cell death and inflammation, while little is known about its roles in COPD. Here, we demonstrate that GRP78 regulates CS-induced necroptosis and injury in bronchial epithelial cells. Materials and methods: GRP78 and necroptosis markers were examined in human bronchial epithelial (HBE) cell line, primary mouse tracheal epithelial cells, and mouse lungs. siRNA targeting GRP78 gene and necroptosis inhibitor were used. Expression of inflammatory cytokines, mucin MUC5AC, and related signaling pathways were detected. Results: Exposure to CS significantly increased the expression of GRP78 and necroptosis markers in HBE cell line, primary mouse tracheal epithelial cells, and mouse lungs. Inhibition of GRP78 significantly suppressed CS extract (CSE)-induced necroptosis. Furthermore, GRP78-necroptosis cooperatively regulated CSE-induced inflammatory cytokines such as interleukin 6 (IL6), IL8, and mucin MUC5AC in HBE cells, likely through the activation of nuclear factor (NF-κB) and activator protein 1 (AP-1) pathways, respectively. Conclusion: Taken together, our results demonstrate that GRP78 promotes CSE-induced inflammatory response and mucus hyperproduction in airway epithelial cells, likely through upregulation of necroptosis and subsequent activation of NF-κB and AP-1 pathways. Thus, inhibition of GRP78 and/or inhibition of necroptosis could be the effective therapeutic approaches for the treatment of COPD.
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.