ReviewCells2022
Impaired Alveolar Re-Epithelialization in Pulmonary Emphysema.
Review in Cells, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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
19 citing papers in PubMed, 33 citations in OpenAlex.
- Co-localization of TAZ and H2A.Z up-regulates IL-6 expression in alveolar epithelial cells to polarize M2 cells to alleviate hypoxia-induced lung injury.Genes & diseases · 2026Article
- Attenuated FTO induces necroptosis of alveolar epithelium via the mRedox biology · 2026Article
- Dysregulated ITGA3/FAK/YAP axis mediates impaired alveolar type II epithelial cells function in COPD.Journal of advanced research · 2026Article
- Cryptochrome Loss Drives COPD-like Lung Pathology through Disrupted Alveolar Epithelial Proliferation and Immune Homeostasis.bioRxiv : the preprint server for biology · 2026Article
- Regenerative therapeutics for chronic obstructive pulmonary disease.Pharmacological reviews · 2026Review
- Epigenetic dysregulation of IRF9 drives excessive interferon signaling in COPD.EMBO molecular medicine · 2026Article
- New approaches to uncover COPD pathobiology and develop therapies.JCI insight · 2026Review
- Review
- Artificial intelligence-guided design of lipid nanoparticles for pulmonary gene therapy.Nature biotechnology · 2025Article
- Wenshen Yiqi Granule Alleviates Chronic Obstructive Pulmonary Disease via the Long Noncoding RNA-XIST/MicroRNA-200c-3p Axis.Pulmonary circulation · 2025Article
- Role of Ferroptosis in Alveolar Epithelial Cells in Acute Respiratory Distress Syndrome.Journal of inflammation research · 2025Review
- Lung repair and regeneration: Advanced models and insights into human disease.Cell stem cell · 2024Review
- Alveolar Epithelial Cell Dysfunction in Idiopathic Pulmonary Fibrosis Linked to Lipid Alterations: Therapeutic Implications.American journal of respiratory cell and molecular biology · 2024Article
- The Regulation of Fatty Acid Synthase by Exosomal miR-143-5p and miR-342-5p in Idiopathic Pulmonary Fibrosis.American journal of respiratory cell and molecular biology · 2024Article
- Epithelial stem cells and niches in lung alveolar regeneration and diseases.Chinese medical journal pulmonary and critical care medicine · 2024Article
- MiR-23a-3p alleviates cigarette smoke extract-induced pulmonary vascular endothelial cell apoptosis by targeting DNAJB1 in emphysema.The clinical respiratory journal · 2023Article
- Cytokine signaling converging onFrontiers in immunology · 2023Article
- Loss of E-cadherin is causal to pathologic changes in chronic lung disease.Communications biology · 2022Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Alveolar type II (ATII) cells are progenitors in alveoli and can repair the alveolar epithelium after injury. They are intertwined with the microenvironment for alveolar epithelial cell homeostasis and re-epithelialization. A variety of ATII cell niches, transcription factors, mediators, and signaling pathways constitute a specific environment to regulate ATII cell function. Particularly, WNT/β-catenin, YAP/TAZ, NOTCH, TGF-β, and P53 signaling pathways are dynamically involved in ATII cell proliferation and differentiation, although there are still plenty of unknowns regarding the mechanism. However, an imbalance of alveolar cell death and proliferation was observed in patients with pulmonary emphysema, contributing to alveolar wall destruction and impaired gas exchange. Cigarette smoking causes oxidative stress and is the primary cause of this disease development. Aberrant inflammatory and oxidative stress responses result in loss of cell homeostasis and ATII cell dysfunction in emphysema. Here, we discuss the current understanding of alveolar re-epithelialization and altered reparative responses in the pathophysiology of this disease. Current therapeutics and emerging treatments, including cell therapies in clinical trials, are addressed as well.
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.