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

Cardiac aging is initiated by matrix metalloproteinase-9-mediated endothelial dysfunction.

American journal of physiology. Heart and circulatory physiology - 15 May 2014

Yabluchanskiy Andriy, Ma Yonggang, Chiao Ying Ann, Lopez Elizabeth F, Voorhees Andrew P, Toba Hiroe, Hall Michael E, Han Hai-Chao, Lindsey Merry L, Jin Yu-Fang

Abstract excerpt

Aging is linked to increased matrix metalloproteinase-9 (MMP-9) expression and extracellular matrix turnover, as well as a decline in function of the left ventricle (LV). Previously, we demonstrated that C57BL/6J wild-type (WT) mice > 18 mo of age show impaired diastolic function, which was atten...

Read the complete abstract on PubMed

Topics

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

Share to Endothelium, Vascular
Share to Heart
Share to Hypertrophy

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Matrix Metalloproteinase 9

Share to Models, Animal

Share to Neovascularization, Physiologic

Share to Ventricular Dysfunction, Left

Share to Ventricular Remodeling

Source

Open in PubMed Open full text

Identifiers

PMID: 24658018
DOI: 10.1152/ajpheart.00090.2014
PMCID: PMC4024719

Genes

CCR10

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 4 Sept 2026. Prepared record publication-24658018-2026-09-04.2. Manifest publication-graph-cohort-2026-09-04.2.

Source receipt: PubMed via Helena Literature Corpus, retrieved 4 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Cardiac aging is initiated by matrix metalloproteinase-9-mediated endothelial dysfunction.PMID 24658018Read ↗

Macrophage overexpression of matrix metalloproteinase-9 in aged mice improves diastolic physiology and cardiac wound healing after myocardial infarction.Semantic proximity Read ↗

Myocardial Infarction Superimposed on Aging: MMP-9 Deletion Promotes M2 Macrophage PolarizationSemantic proximity Read ↗

Matrix metalloproteinase-9 deletion attenuates myocardial fibrosis and diastolic dysfunction in ageing mice.Semantic proximity Read ↗

Deriving a cardiac ageing signature to reveal MMP-9-dependent inflammatory signalling in senescence.Semantic proximity Read ↗

Targeted deletion of MMP-9 attenuates myocardial contractile dysfunction in heart failure.Semantic proximity Read ↗

Cardiomyocyte-specific Bmal1 deletion in mice triggers diastolic dysfunction, extracellular matrix response, and impaired resolution of inflammation.Semantic proximity Read ↗

Remodeling of the Cardiac Extracellular Matrix Proteome During Chronological and Pathological AgingSemantic proximity Read ↗

p38β/MAPK11 Deficiency Exacerbates Cardiac Structural and Electrophysiological Remodeling and Contributes to Immune Dysregulation in the Aging HeartSemantic proximity Read ↗

Proteomic analysis identifies <i>in vivo</i> candidate matrix metalloproteinase‐9 substrates in the left ventricle post‐myocardial infarctionSemantic proximity Read ↗

Collagen XV is necessary for modeling of the extracellular matrix and its deficiency predisposes to cardiomyopathy.Semantic proximity Read ↗

LXR/RXR signaling and neutrophil phenotype following myocardial infarction classify sex differences in remodeling.Semantic proximity Read ↗

EMC10 (Endoplasmic Reticulum Membrane Protein Complex Subunit 10) Is a Bone Marrow-Derived Angiogenic Growth Factor Promoting Tissue Repair After Myocardial Infarction.Semantic proximity Read ↗

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