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

Potential molecular mechanism of cardiac hypertrophy in mice induced by exposure to ambient PM2.5

19 Aug 2021

Abstract excerpt

Cardiac hypertrophy could be induced by ambient fine particulate matter (PM2.5) exposure. Since cardiac hypertrophy represents an early event leading to heart dysfunction, it is necessary to explore the molecular mechanisms, which are largely unknown. In the present study, an ambient particulate matter exposure mice model was established to explore its adverse effects related to the heart and the potential...

Read the complete abstract on PubMed

Topics

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

Share to Air Quality and Health Impacts
Share to Cardiovascular Disease and Adiposity
Share to Circular RNAs in diseases

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 34418850
DOI: 10.1016/j.ecoenv.2021.112659

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 8 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Potential molecular mechanism of cardiac hypertrophy in mice induced by exposure to ambient PM2.5PMID 34418850Read ↗

Biochemical Evidence of PM2.5 Critical Components in the Induction of Myocardial Fibrosis in MiceSemantic proximity Read ↗

Cardiovascular remodeling in response to long-term exposure to fine particulate matter air pollution.Semantic proximity Read ↗

Fine particulate matter‑induced cardiac developmental toxicity (Review)Semantic proximity Read ↗

Particulate matter-induced epigenetic modifications and lung complications.Semantic proximity Read ↗

Assessment on the lung injury of mice posed by airborne PM2.5 collected from developing area in China and associated molecular mechanisms: from histopathology to integrated transcriptome analysisSemantic proximity Read ↗

PM2.5 promotes the phenotypic transition of vascular smooth muscle cells in atherosclerosis by activating pro-ferroptotic signaling via DRP1/PINK1/Parkin-dependent mitophagy.Semantic proximity Read ↗

Fine particulate matter 2.5 exerted its toxicological effect by regulating a new layer, long non-coding RNA.Semantic proximity Read ↗

Maternal PM2.5 Exposure and Cardiac Developmental Abnormalities in Fetuses and Neonates: Progressive Activation of the Complement and Coagulation CascadeSemantic proximity Read ↗

Risks of Respiratory and Circulatory System Diseases Induced by Exposure to PM2.5 in High Humidity and Low Solar Radiation Environments: Disease Types, Genes, and FunctionsSemantic proximity Read ↗

Microarray analysis of mRNA expression profiles in liver of ob/ob mice with real-time atmospheric PM2.5 exposureSemantic proximity Read ↗

NO2 exposure contributes to cardiac hypertrophy in male mice through apoptosis signaling pathwaysSemantic proximity Read ↗

Molecular mechanism of Pulmonary diseases caused by exposure to urban PM2.5 in Chengdu-Chongqing Economic Circle, ChinaSemantic proximity Read ↗

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