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

Monoamine oxidase-A is a novel driver of stress-induced premature senescence through inhibition of parkin-mediated mitophagy.

Aging cell - 1 Oct 2018

Manzella Nicola, Santin Yohan, Maggiorani Damien, Martini Hélène, Douin-Echinard Victorine, Passos Joao F, Lezoualc'h Frank, Binda Claudia, Parini Angelo, Mialet-Perez Jeanne

Abstract excerpt

Cellular senescence, the irreversible cell cycle arrest observed in somatic cells, is an important driver of age-associated diseases. Mitochondria have been implicated in the process of senescence, primarily because they are both sources and targets of reactive oxygen species (ROS). In the heart, oxidative stress contributes to pathological cardiac ageing, but the mechanisms underlying ROS production are still...

Read the complete abstract on PubMed

Topics

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

Share to Cellular Senescence
Share to Cyclin-Dependent Kinase Inhibitor p16

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Cyclin-Dependent Kinase Inhibitor p21

Share to Mitophagy

Share to Monoamine Oxidase

Share to Myocytes, Cardiac

Share to Sirolimus

Share to TOR Serine-Threonine Kinases

Source

Open in PubMed Open full text

Identifiers

PMID: 30003648
DOI: 10.1111/acel.12811
PMCID: PMC6156293

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 6 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Monoamine oxidase-A is a novel driver of stress-induced premature senescence through inhibition of parkin-mediated mitophagy.PMID 30003648Read ↗

Mitochondria, Oxidative Stress and the Kynurenine System, with a Focus on Ageing and Neuroprotection.Semantic proximity Read ↗

Selective Cardiomyocyte Oxidative Stress Leads to Bystander Senescence of Cardiac Stromal CellsSemantic proximity Read ↗

Mitochondrial dysfunction in cell senescence and aging.Semantic proximity Read ↗

Targeting Mitochondria to Control Ageing and SenescenceSemantic proximity Read ↗

Suppressed basal mitophagy drives cellular aging phenotypes that can be reversed by a p62-targeting small molecule.Semantic proximity Read ↗

Mitochondrial Dysfunction Meets Senescence.Semantic proximity Read ↗

Mitochondria in Cell Senescence: Is Mitophagy the Weakest Link?Semantic proximity Read ↗

Cellular Senescence, Mitochondrial Dysfunction, and Their Link to Cardiovascular DiseaseSemantic proximity Read ↗

Role of mitochondrial dysfunction and altered autophagy in cardiovascular aging and disease: from mechanisms to therapeuticsSemantic proximity Read ↗

Oncogene-induced senescence mitochondrial metabolism and bioenergetics drive the secretory phenotype: further characterization and comparison with other senescence-inducing stimuliSemantic proximity Read ↗

Contribution of Impaired Mitochondrial Autophagy to Cardiac AgingSemantic proximity Read ↗

Mitochondria are required for pro-ageing features of the senescent phenotype.Semantic proximity Read ↗

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