ArticleAging cell2018
Vascular smooth muscle cells direct extracellular dysregulation in aortic stiffening of hypertensive rats.
Article in Aging cell, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
23 citing papers in PubMed, 38 citations in OpenAlex.
- Cellular Heterogeneity During Arterial Aging.Aging cell · 2026Review
- Vascular Mechanobiology: From Membrane to Nucleus.Advances in experimental medicine and biology · 2026Review
- New insights into the pharmacological inhibition of SRF activity: Key inhibitory targets and mechanisms.Vascular pharmacology · 2024Review
- Recent advances in serum response factor posttranslational modifications and their therapeutic potential in cardiovascular and neurological diseases.Vascular pharmacology · 2024Review
- Effects of vasoactive substances on biomechanics of small resistance arteries of male and female Dahl salt-sensitive rats.Pharmacology research & perspectives · 2024Article
- Two methods of isolation of rat aortic smooth muscle cells with high yield.Biology methods & protocols · 2024Article
- Survivin regulates intracellular stiffness and extracellular matrix production in vascular smooth muscle cells.APL bioengineering · 2023Article
- Age and Blood Pressure Contribute to Aortic Cell and Tissue Stiffness Through Distinct Mechanisms.Hypertension (Dallas, Tex. : 1979) · 2022Article
- SRF: a seriously responsible factor in cardiac development and disease.Journal of biomedical science · 2022Review
- Lysyl oxidase promotes anaplastic thyroid carcinoma cell proliferation and metastasis mediated via BMP1.Gland surgery · 2022Article
- Extracellular Matrix in Aging Aorta.Frontiers in cell and developmental biology · 2022Review
- Article
- Hsp22 Deficiency Induces Age-Dependent Cardiac Dilation and Dysfunction by Impairing Autophagy, Metabolism, and Oxidative Response.Antioxidants (Basel, Switzerland) · 2021Article
- Single-cell RNA-seq reveals cellular heterogeneity of mouse carotid artery under disturbed flow.Cell death discovery · 2021Article
- Serum response factor-cofactor interactions and their implications in disease.The FEBS journal · 2021Review
- The Progress of Advanced Ultrasonography in Assessing Aortic Stiffness and the Application Discrepancy between Humans and Rodents.Diagnostics (Basel, Switzerland) · 2021Review
- Molecular Mechanisms of Leukocyte Migration and Its Potential Targeting-Lessons Learned From MKL1/SRF-Related Primary Immunodeficiency Diseases.Frontiers in immunology · 2021Review
- Hypoxic modulation of fetal vascular MLCK abundance, localization, and function.American journal of physiology. Regulatory, integrative and comparative physiology · 2021Article
- New progress on the study of aortic stiffness in age-related hypertension.Journal of hypertension · 2020Review
- Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Aortic stiffening is an independent risk factor that underlies cardiovascular morbidity in the elderly. We have previously shown that intrinsic mechanical properties of vascular smooth muscle cells (VSMCs) play a key role in aortic stiffening in both aging and hypertension. Here, we test the hypothesis that VSMCs also contribute to aortic stiffening through their extracellular effects. Aortic stiffening was confirmed in spontaneously hypertensive rats (SHRs) vs. Wistar-Kyoto (WKY) rats in vivo by echocardiography and ex vivo by isometric force measurements in isolated de-endothelized aortic vessel segments. Vascular smooth muscle cells were isolated from thoracic aorta and embedded in a collagen I matrix in an in vitro 3D model to form reconstituted vessels. Reconstituted vessel segments made with SHR VSMCs were significantly stiffer than vessels made with WKY VSMCs. SHR VSMCs in the reconstituted vessels exhibited different morphologies and diminished adaptability to stretch compared to WKY VSMCs, implying dual effects on both static and dynamic stiffness. SHR VSMCs increased the synthesis of collagen and induced collagen fibril disorganization in reconstituted vessels. Mechanistically, compared to WKY VSMCs, SHR VSMCs exhibited an increase in the levels of active integrin β1- and bone morphogenetic protein 1 (BMP1)-mediated proteolytic cleavage of lysyl oxidase (LOX). These VSMC-induced alterations in the SHR were attenuated by an inhibitor of serum response factor (SRF)/myocardin. Therefore, SHR VSMCs exhibit extracellular dysregulation through modulating integrin β1 and BMP1/LOX via SRF/myocardin signaling in aortic stiffening.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.