ArticleHypertension (Dallas, Tex. : 1979)2016
Age- and Hypertension-Associated Protein Aggregates in Mouse Heart Have Similar Proteomic Profiles.
Article in Hypertension (Dallas, Tex. : 1979), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.
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Who cites it
60 citing papers in PubMed, 89 citations in OpenAlex.
- Proteostasis of organelles in aging and disease.The FEBS journal · 2026Review
- Cardiac ageing: from hallmarks to therapeutic opportunities.Cardiovascular research · 2025Review
- Altered protein homeostasis in cardiovascular diseases contributes to Alzheimer's-like neuropathology.Basic research in cardiology · 2025Article
- UBE2V1 governs aging induced protein aggregation and developmental defects in oocytes and embryos.Communications biology · 2025Article
- Proteostatic Imbalance Drives the Pathogenesis and Age-Related Exacerbation of Heart Failure With Preserved Ejection Fraction.JACC. Basic to translational science · 2025Article
- Hyperactive mTORC1/4EBP1 signaling dysregulates proteostasis and accelerates cardiac aging.GeroScience · 2025Article
- Small Heat Shock Proteins: Protein Aggregation Amelioration and Neuro- and Age-Protective Roles.International journal of molecular sciences · 2025Review
- Unveiling the molecular and cellular links between obstructive sleep apnea-hypopnea syndrome and vascular aging.Chinese medical journal · 2025Review
- Proteostasis Decline and Redox Imbalance in Age-Related Diseases: The Therapeutic Potential of NRF2.Biomolecules · 2025Review
- Myocardial infarction elevates endoplasmic reticulum stress and protein aggregation in heart as well as brain.Molecular and cellular biochemistry · 2024Article
- Exercise training decreases the load and changes the content of circulating SDS-resistant protein aggregates in patients with heart failure with reduced ejection fraction.Molecular and cellular biochemistry · 2024Article
- Phosphorylation-Regulated Dynamic Phase Separation of HIP-55 Protects Against Heart Failure.Circulation · 2024Article
- Alzheimer's-specific brain amyloid interactome: Neural-network analysis of intra-aggregate crosslinking identifies novel drug targets.iScience · 2024Article
- Can salivary and skin microbiome become a biodetector for aging-associated diseases? Current insights and future perspectives.Frontiers in aging · 2024Review
- Ezetimibe Lowers Risk of Alzheimer's and Related Dementias over Sevenfold, Reducing Aggregation in Model Systems by Inhibiting 14-3-3G::Hexokinase Interaction.Aging biology · 2024Article
- Hallmarks of cardiovascular ageing.Nature reviews. Cardiology · 2023Review
- A safety mechanism enables tissue-specific resistance to protein aggregation during aging in C. elegans.PLoS biology · 2023Article
- Characterization of Plasma SDS-Protein Aggregation Profile of Patients with Heart Failure with Preserved Ejection Fraction.Journal of cardiovascular translational research · 2023Article
- Proteomics analysis in myocardium of spontaneously hypertensive rats.Scientific reports · 2023Article
- Protein homeostasis in the aged and diseased heart.The journal of cardiovascular aging · 2023Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
Neurodegenerative diseases are largely defined by protein aggregates in affected tissues. Aggregates contain some shared components as well as proteins thought to be specific for each disease. Aggregation has not previously been reported in the normal, aging heart or the hypertensive heart. Detergent-insoluble protein aggregates were isolated from mouse heart and characterized on 2-dimensional gels. Their levels increased markedly and significantly with aging and after sustained angiotensin II-induced hypertension. Of the aggregate components identified by high-resolution proteomics, half changed in abundance with age (392/787) or with sustained hypertension (459/824), whereas 30% (273/901) changed concordantly in both, each P<0.05. One fifth of these proteins were previously associated with age-progressive neurodegenerative or cardiovascular diseases, or both (eg, ApoE, ApoJ, ApoAIV, clusterin, complement C3, and others involved in stress-response and protein-homeostasis pathways). Because fibrosis is a characteristic of both aged and hypertensive hearts, we posited that aging of fibroblasts may contribute to the aggregates observed in cardiac tissue. Indeed, as cardiac myofibroblasts "senesced" (approached their replicative limit) in vitro, they accrued aggregates with many of the same constituent proteins observed in vivo during natural aging or sustained hypertension. In summary, we have shown for the first time that compact (detergent-insoluble) protein aggregates accumulate during natural aging, chronic hypertension, and in vitro myofibroblast senescence, sharing many common proteins. Thus, aggregates that arise from disparate causes (aging, hypertension, and replicative senescence) may have common underlying mechanisms of accrual.
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