Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

TROP2 promotes PINK1-mediated mitophagy and apoptosis to accelerate the progression of senile chronic obstructive pulmonary disease by up-regulating DRP1 expression

29 Apr 2024

Abstract excerpt

Chronic obstructive pulmonary disease (COPD) is a chronic airway inflammatory disease characterised by irreversible airflow limitation. The elderly are a vulnerable population for developing COPD. With the growth of age, physiological degenerative changes occur in the thorax, bronchus, lung and vascular wall, which can lead to age-related physiological attenuation of lung function in the elderly, so the...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Autophagy in Disease and Therapy
Share to Chronic Obstructive Pulmonary Disease (COPD) Research
Share to Interstitial Lung Diseases and Idiopathic Pulmonary Fibrosis

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 38685507
DOI: 10.1016/j.exger.2024.112441

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

TROP2 promotes PINK1-mediated mitophagy and apoptosis to accelerate the progression of senile chronic obstructive pulmonary disease by up-regulating DRP1 expressionPMID 38685507Read ↗

PINK1-PARK2-mediated mitophagy in COPD and IPF pathogenesesSemantic proximity Read ↗

PINK1-mediated Mitophagy Contributes to Pulmonary Vascular Remodeling in Pulmonary HypertensionSemantic proximity Read ↗

Mitochondrial dysfunction in inflammatory responses and cellular senescence: pathogenesis and pharmacological targets for chronic lung diseasesSemantic proximity Read ↗

PRKN-regulated mitophagy and cellular senescence during COPD pathogenesisSemantic proximity Read ↗

Involvement of NEAT1/PINK1-mediated mitophagy in chronic obstructive pulmonary disease induced by cigarette smoke or PM2.5Semantic proximity Read ↗

PINK1 attenuates mtDNA release in alveolar epithelial cells and TLR9 mediated profibrotic responsesSemantic proximity Read ↗

Accelerated lung aging and chronic obstructive pulmonary diseaseSemantic proximity Read ↗

Age-dependent assessment of genes involved in cellular senescence, telomere and mitochondrial pathways in human lung tissue of smokers, COPD and IPF: Associations with SARS-CoV-2 COVID-19 ACE2-TMPRSS2-Furin-DPP4 axisSemantic proximity Read ↗

Knockdown of RTEL1 Alleviates Chronic Obstructive Pulmonary Disease by Modulating M1, M2 Macrophage Polarization and InflammationSemantic proximity Read ↗

Age-dependent assessment of genes involved in cellular senescence, telomere and mitochondrial pathways in human lung tissue of smokers, COPD and IPF: Associations with SARS-CoV-2 COVID-19 ACE2-TMPRSS2-Furin-DPP4 axisSemantic proximity Read ↗

Current views in chronic obstructive pulmonary disease pathogenesis and managementSemantic proximity Read ↗

Identification and validation of aging-related genes in COPD based on bioinformatics analysisSemantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.