ReviewCanadian journal of physiology and pharmacology2015
Interaction between endoplasmic/sarcoplasmic reticulum stress (ER/SR stress), mitochondrial signaling and Ca(2+) regulation in airway smooth muscle (ASM).
Review in Canadian journal of physiology and pharmacology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 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
30 citing papers in PubMed, 42 citations in OpenAlex.
- Mechanically induced dysregulation of calcium homeostasis: a molecular linchpin in asthmatic pathogenesis.European journal of medical research · 2025Review
- Salivary mitofusin levels in periodontal disease: a cross-sectional case-control study.BMC oral health · 2025Article
- Targeting ER stress in skeletal muscle through physical activity: a strategy for combating neurodegeneration-associated muscle decline.Frontiers in molecular neuroscience · 2025Review
- Nicotine affects mitochondrial structure and function in human airway smooth muscle cells.American journal of physiology. Lung cellular and molecular physiology · 2023Article
- Fine particulate matter promotes airway inflammation and mucin production by activating endoplasmic reticulum stress and the IRE1α/NOD1/NF‑κB pathway.International journal of molecular medicine · 2023Article
- Cell-Based Measurement of Mitochondrial Function in Human Airway Smooth Muscle Cells.International journal of molecular sciences · 2023Article
- Desert particulate matter from Afghanistan increases airway obstruction in human distal lungs exposed to type 2 cytokine IL-13.Frontiers in medicine · 2023Article
- Bronchial smooth muscle cell in asthma: where does it fit?BMJ open respiratory research · 2022Review
- Mitochondria signaling pathways in allergic asthma.Journal of investigative medicine : the official publication of the American Federation for Clinical Research · 2022Review
- STIM1 is a core trigger of airway smooth muscle remodeling and hyperresponsiveness in asthma.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Nicotinic α7 acetylcholine receptor (α7nAChR) in human airway smooth muscle.Archives of biochemistry and biophysics · 2021Article
- Systems Approaches to Treatment Response to Imatinib in Severe Asthma: A Pilot Study.Journal of personalized medicine · 2021Article
- TNFα induces mitochondrial fragmentation and biogenesis in human airway smooth muscle.American journal of physiology. Lung cellular and molecular physiology · 2021Article
- Inflammation-Induced Protein Unfolding in Airway Smooth Muscle Triggers a Homeostatic Response in Mitochondria.International journal of molecular sciences · 2020Review
- Inhibiting ER Stress Weakens Neuronal Pyroptosis in a Mouse Acute Hemorrhagic Stroke Model.Molecular neurobiology · 2020Article
- TNFα selectively activates the IRE1α/XBP1 endoplasmic reticulum stress pathway in human airway smooth muscle cells.American journal of physiology. Lung cellular and molecular physiology · 2020Article
- Mitochondrial biology in airway pathogenesis and the role of NRF2.Archives of pharmacal research · 2020Review
- A Putative Prohibitin-Calcium Nexus inJournal of diabetes research · 2020Review
- Update on the role of endoplasmic reticulum stress in asthma.American journal of translational research · 2020Review
- Endoplasmic Reticulum Stress Induces MUC5AC and MUC5B Expression in Human Nasal Airway Epithelial Cells.Clinical and experimental otorhinolaryngology · 2019Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Airway inflammation is a key aspect of diseases such as asthma. Several inflammatory cytokines (e.g., TNFα and IL-13) increase cytosolic Ca(2+) ([Ca(2+)]cyt) responses to agonist stimulation and Ca(2+) sensitivity of force generation, thereby enhancing airway smooth muscle (ASM) contractility (hyper-reactive state). Inflammation also induces ASM proliferation and remodeling (synthetic state). In normal ASM, the transient elevation of [Ca(2+)]cyt induced by agonists leads to a transient increase in mitochondrial Ca(2+) ([Ca(2+)]mito) that may be important in matching ATP production with ATP consumption. In human ASM (hASM) exposed to TNFα and IL-13, the transient increase in [Ca(2+)]mito is blunted despite enhanced [Ca(2+)]cyt responses. We also found that TNFα and IL-13 induce reactive oxidant species (ROS) formation and endoplasmic/sarcoplasmic reticulum (ER/SR) stress (unfolded protein response) in hASM. ER/SR stress in hASM is associated with disruption of mitochondrial coupling with the ER/SR membrane, which relates to reduced mitofusin 2 (Mfn2) expression. Thus, in hASM it appears that TNFα and IL-13 result in ROS formation leading to ER/SR stress, reduced Mfn2 expression, disruption of mitochondrion-ER/SR coupling, decreased mitochondrial Ca(2+) buffering, mitochondrial fragmentation, and increased cell proliferation.
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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.