ReviewFrontiers in cell and developmental biology2019
Endoplasmic Reticulum Stress and Mitochondrial Function in Airway Smooth Muscle.
Review in Frontiers in cell and developmental biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 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.
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Who cites it
40 citing papers in PubMed, 63 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
- ER-mitochondria contact sites and organelle stress in asthma.Molecular biology reports · 2026Review
- AhR activation inhibits DRP1-induced mitochondrial fission in airway smooth muscle during asthma.American journal of respiratory cell and molecular biology · 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
- The Role of Aryl Hydrocarbon Receptor in Airway Remodeling: Mechanistic Insights Across Cellular Functions.Clinical reviews in allergy & immunology · 2026Review
- Nandrolone Abuse Prior to Head Trauma Mitigates Endoplasmic Reticulum Stress, Mitochondrial Bioenergetic Deficits, and Markers of Neurodegeneration.Molecular neurobiology · 2025Article
- Autistic behavior is a common outcome of biallelic disruption of PDZD8 in humans and mice.Molecular autism · 2025Article
- Endoplasmic reticulum stress in lung cancer.Frontiers in oncology · 2025Review
- Exogenous SPD inhibits trastuzumab-mediated cardiomyocyte pyroptosis through SIRT3-regulated mitochondrial quality control.International journal of biological sciences · 2025Article
- Multifaceted roles of mitochondria in asthma.Cell biology and toxicology · 2024Review
- Evaluation of cadmium effects on the glucose metabolism on insulin resistance HepG2 cells.Heliyon · 2024Article
- Celastrol alleviates atopic dermatitis by regulating Ezrin-mediated mitochondrial fission and fusion.Journal of cellular and molecular medicine · 2024Article
- N-cadherin Alleviates Apoptosis and Senescence of Nucleus Pulposus Cells via Suppressing ROS-dependent ERS in the Hyper-osmolarity Microenvironment.International journal of medical sciences · 2024Article
- Increased Ca2 + transport across the mitochondria-associated membranes by Mfn2 inhibiting endoplasmic reticulum stress in ischemia/reperfusion kidney injury.Scientific reports · 2023Article
- Mitochondrial dynamics modulate the allergic inflammation in a murine model of allergic rhinitis.Immunity, inflammation and disease · 2023Article
- Cell-Based Measurement of Mitochondrial Function in Human Airway Smooth Muscle Cells.International journal of molecular sciences · 2023Article
- Inhibition of DRP1-dependent mitochondrial fission by Mdivi-1 alleviates atherosclerosis through the modulation of M1 polarization.Journal of translational medicine · 2023Article
- Peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α) overexpression alleviates endoplasmic reticulum stress after acute kidney injury.Renal failure · 2022Article
- Mitochondrial adaptations to inactivity in diaphragm muscle fibers.Journal of applied physiology (Bethesda, Md. : 1985) · 2022Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Inflammatory airway diseases such as asthma affect more than 300 million people world-wide. Inflammation triggers pathophysiology via such as tumor necrosis factor α (TNFα) and interleukins (e.g., IL-13). Hypercontraction of airway smooth muscle (ASM) and ASM cell proliferation are major contributors to the exaggerated airway narrowing that occurs during agonist stimulation. An emergent theme in this context is the role of inflammation-induced endoplasmic reticulum (ER) stress and altered mitochondrial function including an increase in the formation of reactive oxygen species (ROS). This may establish a vicious cycle as excess ROS generation leads to further ER stress. Yet, it is unclear whether inflammation-induced ROS is the major mechanism leading to ER stress or the consequence of ER stress. In various diseases, inflammation leads to an increase in mitochondrial fission (fragmentation), associated with reduced levels of mitochondrial fusion proteins, such as mitofusin 2 (Mfn2). Mitochondrial fragmentation may be a homeostatic response since it is generally coupled with mitochondrial biogenesis and mitochondrial volume density thereby reducing demand on individual mitochondrion. ER stress is triggered by the accumulation of unfolded proteins, which induces a homeostatic response to alter protein balance via effects on protein synthesis and degradation. In addition, the ER stress response promotes protein folding via increased expression of molecular chaperone proteins. Reduced Mfn2 and altered mitochondrial dynamics may not only be downstream to ER stress but also upstream such that a reduction in Mfn2 triggers further ER stress. In this review, we summarize the current understanding of the link between inflammation-induced ER stress and mitochondrial function and the role played in the pathophysiology of inflammatory airway diseases.
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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.