ArticleNature aging2023
The age of bone marrow dictates the clonality of smooth muscle-derived cells in atherosclerotic plaques.
Article in Nature aging, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 29 citations in OpenAlex.
- Aged murine bone marrow myeloid and mesenchymal cells develop unique senescence phenotypes.The Journal of clinical investigation · 2026Article
- Smooth muscle cell phenotypic modulation during atherosclerosis.Vascular pharmacology · 2026Review
- Research progress on targeted regulatory proteins in the prevention and treatment of atherosclerosis.Frontiers in immunology · 2026Review
- The systemic costs of hematopoietic stem cell aging.Development (Cambridge, England) · 2025Review
- Roadmap for alleviating the manifestations of ageing in the cardiovascular system.Nature reviews. Cardiology · 2025Review
- Age-Related Impairments in Immune Cell Efferocytosis and Autophagy Hinder Atherosclerosis Regression.Arteriosclerosis, thrombosis, and vascular biology · 2025Article
- Periarteriolar niches become inflamed in aging bone marrow, remodeling the stromal microenvironment and depleting lymphoid progenitors.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Bone Marrow Niche in Cardiometabolic Disease: Mechanisms and Therapeutic Potential.Circulation research · 2025Review
- Chronic inflammation and vascular cell plasticity in atherosclerosis.Nature cardiovascular research · 2024Review
- A Concept of "Athero-Oncology": Tumor-Like Smooth Muscle Cells Drive Atherosclerosis.Circulation · 2024Article
- Atherosclerosis Is a Smooth Muscle Cell-Driven Tumor-Like Disease.Circulation · 2024Article
- Integrins as Drug Targets in Vascular and Related Diseases.International journal of drug discovery and pharmacology · 2024Article
- Systemic and local regulation of hematopoietic homeostasis in health and disease.Nature cardiovascular research · 2024Review
- Resolvin D2 limits atherosclerosis progression via myeloid cell-GPR18.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024Article
- Manifestations of human atherosclerosis across vascular beds.JVS-vascular insights · 2024Article
- Clonal Expansion in Cardiovascular Pathology.JACC. Basic to translational science · 2024Review
- Hallmarks of cardiovascular ageing.Nature reviews. Cardiology · 2023Review
- Missing checkpoints in premature aging.Nature aging · 2023Article
- Article
- Role of vascular smooth muscle cell clonality in atherosclerosis.Frontiers in cardiovascular medicine · 2023Review
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16 authors at 1 institution in 1 country.
Funding
Abstract
Aging is the predominant risk factor for atherosclerosis, the leading cause of death. Rare smooth muscle cell (SMC) progenitors clonally expand giving rise to up to ~70% of atherosclerotic plaque cells; however, the effect of age on SMC clonality is not known. Our results indicate that aged bone marrow (BM)-derived cells non-cell autonomously induce SMC polyclonality and worsen atherosclerosis. Indeed, in myeloid cells from aged mice and humans, TET2 levels are reduced which epigenetically silences integrin β3 resulting in increased tumor necrosis factor [TNF]-α signaling. TNFα signals through TNF receptor 1 on SMCs to promote proliferation and induces recruitment and expansion of multiple SMC progenitors into the atherosclerotic plaque. Notably, integrin β3 overexpression in aged BM preserves dominance of the lineage of a single SMC progenitor and attenuates plaque burden. Our results demonstrate a molecular mechanism of aged macrophage-induced SMC polyclonality and atherogenesis and suggest novel therapeutic strategies.
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