ArticleNature communications2021
PGC-1α mediates a metabolic host defense response in human airway epithelium during rhinovirus infections.
Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 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
28 citing papers in PubMed, 46 citations in OpenAlex.
- BVDV utilizes PGC-1α downregulation to remodel the mitochondrial metabolic microenvironment, enhancing viral replication and impairing host immunity.Frontiers in veterinary science · 2026Article
- Parechovirus-3 infection disrupts immunometabolism and leads to glutamate excitotoxicity in neural organoids.Cellular and molecular life sciences : CMLS · 2025Article
- Striae gravidarum in the Han Chinese pregnant population: identifying genetic markers and risk factors through a prospective cohort study.BMC pregnancy and childbirth · 2025Article
- Zinc Promotes Mitochondrial Health Through PGC-1alpha Enhancing Bacterial Clearance in Macrophages Infected withInternational journal of molecular sciences · 2025Article
- Identification of picornavirus proteins that inhibit de novo nucleotide synthesis during infection.PLoS pathogens · 2025Article
- N-terminomics and proteomics analysis of Calpain-2 reveal key proteolytic processing of metabolic and cell adhesion proteins.Protein science : a publication of the Protein Society · 2025Article
- Targeting Non-Eosinophilic Immunological Pathways in COPD and AECOPD: Current Insights and Therapeutic Strategies.International journal of chronic obstructive pulmonary disease · 2025Review
- Interactions between epithelial mesenchymal plasticity, barrier dysfunction and innate immune pathways shape the genesis of allergic airway disease.Expert review of respiratory medicine · 2025Review
- Article
- Protective effect of interferon type I on barrier function of human airway epithelium during rhinovirus infections in vitro.Scientific reports · 2024Article
- Modulation of nucleotide metabolism by picornaviruses.PLoS pathogens · 2024Article
- Butyrate reduces adherent-invasiveGut microbes · 2023Article
- Poly I:C Pre-Treatment Induced the Anti-Viral Interferon Response in Airway Epithelial Cells.Viruses · 2023Article
- Interferon signaling drives epithelial metabolic reprogramming to promote secondary bacterial infection.PLoS pathogens · 2023Article
- Oxidative stress and ROS-mediated cellular events in RSV infection: potential protective roles of antioxidants.Virology journal · 2023Review
- Rhinovirus C causes heterogeneous infection and gene expression in airway epithelial cell subsets.Mucosal immunology · 2023Article
- Tryptase β regulation of joint lubrication and inflammation via proteoglycan-4 in osteoarthritis.Nature communications · 2023Article
- Modulation of innate immunity in airway epithelium for host-directed therapy.Frontiers in immunology · 2023Review
- Host-directed therapy with 2-deoxy-D-glucose inhibits human rhinoviruses, endemic coronaviruses, and SARS-CoV-2.Journal of virus eradication · 2022Article
- Airway Epithelial Cell Junctions as Targets for Pathogens and Antimicrobial Therapy.Pharmaceutics · 2022Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Human rhinoviruses (HRV) are common cold viruses associated with exacerbations of lower airways diseases. Although viral induced epithelial damage mediates inflammation, the molecular mechanisms responsible for airway epithelial damage and dysfunction remain undefined. Using experimental HRV infection studies in highly differentiated human bronchial epithelial cells grown at air-liquid interface (ALI), we examine the links between viral host defense, cellular metabolism, and epithelial barrier function. We observe that early HRV-C15 infection induces a transitory barrier-protective metabolic state characterized by glycolysis that ultimately becomes exhausted as the infection progresses and leads to cellular damage. Pharmacological promotion of glycolysis induces ROS-dependent upregulation of the mitochondrial metabolic regulator, peroxisome proliferator-activated receptor-γ coactivator 1α (PGC-1α), thereby restoring epithelial barrier function, improving viral defense, and attenuating disease pathology. Therefore, PGC-1α regulates a metabolic pathway essential to host defense that can be therapeutically targeted to rescue airway epithelial barrier dysfunction and potentially prevent severe respiratory complications or secondary bacterial infections.
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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.