ReviewInternational journal of molecular sciences2020
Inflammation-Induced Protein Unfolding in Airway Smooth Muscle Triggers a Homeostatic Response in Mitochondria.
Review in International journal of molecular sciences, 2020. 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
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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
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Who cites it
19 citing papers in PubMed, 21 citations in OpenAlex.
- ROS scavenging mitigates TNFα-induced endoplasmic reticulum stress and mitochondrial fragmentation in human airway smooth muscle.Function (Oxford, England) · 2026Article
- Molecular mechanisms underlying FCCP-induced mitophagy in human airway smooth muscle cells.American journal of physiology. Lung cellular and molecular physiology · 2026Article
- Inflammaging-associated mitochondrial degeneration occurs in hypoglossal motor neurons prior to tongue muscle.GeroScience · 2026Article
- ER-mitochondria contact sites and organelle stress in asthma.Molecular biology reports · 2026Review
- Mechanical force-induced tissue remodelling in a clinically relevant microphysiological model of asthmatic human lungs.Nature biomedical engineering · 2026Article
- Tumor necrosis factor α-induced endoplasmic reticulum stress promotes airway smooth muscle cell proliferation.American journal of physiology. Lung cellular and molecular physiology · 2026Article
- Ambient aromatic hydrocarbons and prostate cancer: mechanistic evidence linking benzene and PAH exposure to tumor progression.Frontiers in cell and developmental biology · 2026Review
- Betanin, a Natural Product from Red Beets, Improves Endothelial Dysfunction through Activation of Autophagy.Current medicinal chemistry · 2026Article
- The role of post-translational modifications in osteonecrosis of the femoral head.Frontiers in cell and developmental biology · 2026Review
- Silibinin's role in counteracting neuronal apoptosis and synaptic dysfunction in Alzheimer's disease models.Apoptosis : an international journal on programmed cell death · 2025Article
- Molecular mechanisms underlying TNFα-induced mitochondrial fragmentation in human airway smooth muscle cells.American journal of physiology. Lung cellular and molecular physiology · 2024Article
- Chemical Chaperone 4-PBA Mitigates Tumor Necrosis Factor Alpha-Induced Endoplasmic Reticulum Stress in Human Airway Smooth Muscle.International journal of molecular sciences · 2023Article
- Cell-Based Measurement of Mitochondrial Function in Human Airway Smooth Muscle Cells.International journal of molecular sciences · 2023Article
- Molecular Mechanisms Underlying TNFα-Induced Mitochondrial Biogenesis in Human Airway Smooth Muscle.International journal of molecular sciences · 2023Article
- Airway Smooth Muscle Cell Mitochondria Damage and Mitophagy in COPD via ERK1/2 MAPK.International journal of molecular sciences · 2022Article
- Insight into the mitochondrial unfolded protein response and cancer: opportunities and challenges.Cell & bioscience · 2022Review
- Hypoxia-inducible factor-1α promotes proliferation of airway smooth muscle cells through miRNA-103-mediated signaling pathway under hypoxia.In vitro cellular & developmental biology. Animal · 2021Article
- Mitochondria and Antibiotics: For Good or for Evil?Biomolecules · 2021Review
- Mitochondrial Dynamics during Development.Newborn (Clarksville, Md.)Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The effects of airway inflammation on airway smooth muscle (ASM) are mediated by pro-inflammatory cytokines such as tumor necrosis factor alpha (TNFα). In this review article, we will provide a unifying hypothesis for a homeostatic response to airway inflammation that mitigates oxidative stress and thereby provides resilience to ASM. Previous studies have shown that acute exposure to TNFα increases ASM force generation in response to muscarinic stimulation (hyper-reactivity) resulting in increased ATP consumption and increased tension cost. To meet this increased energetic demand, mitochondrial O
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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.