The aging venous system: from varicosities to vascular cognitive impairment - PubMed (original) (raw)

Review

The aging venous system: from varicosities to vascular cognitive impairment

Andrea Ágnes Molnár et al. Geroscience. 2021 Dec.

Abstract

Aging-induced pathological alterations of the circulatory system play a critical role in morbidity and mortality of older adults. While the importance of cellular and molecular mechanisms of arterial aging for increased cardiovascular risk in older adults is increasingly appreciated, aging processes of veins are much less studied and understood than those of arteries. In this review, age-related cellular and morphological alterations in the venous system are presented. Similarities and dissimilarities between arterial and venous aging are highlighted, and shared molecular mechanisms of arterial and venous aging are considered. The pathogenesis of venous diseases affecting older adults, including varicose veins, chronic venous insufficiency, and deep vein thrombosis, is discussed, and the potential contribution of venous pathologies to the onset of vascular cognitive impairment and neurodegenerative diseases is emphasized. It is our hope that a greater appreciation of the cellular and molecular processes of vascular aging will stimulate further investigation into strategies aimed at preventing or retarding age-related venous pathologies.

Keywords: Ageing; Aging; Deep vein thrombosis; GeroScience; Varicose veins; Vascular cognitive impairment; Veins; Venous insufficiency.

© 2021. The Author(s).

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Conflict of interest statement

Zoltan Ungvari, MD, PhD, is serving as Consulting Editor of the American Journal of Physiology-Heart and Circulatory Physiology and Editor-in-Chief of GeroScience.

Figures

Fig. 1

Fig. 1

Aging processes identified in veins and their connections to venous pathology. For detailed description and references, see the corresponding chapters. Abbreviations: CK-8, Cytokeratin-8; FVIII, FIX, clot factors VIII and IX; ICAM-1, Intercellular adhesion molecule-1; iNOS, inducible nitrogen monoxide synthase; IL1α, IL6, IL8, interleukins 1alfa, 6, and 8; MCP-1, Monocyte chemotactic protein; MMP-1, MMP-2, MMP-3, Matrix metalloproteinases 1, 2, and 3; PAI-1; PDGF, platelet-derived growth factor; SM-MHC, Smooth muscle heavy chain; TIMP-2, TIMP-3, tissue inhibitor of matrix metalloproteinase 2 and 3; TxA2, thromboxane A2; VCAM-1, Vascular adhesion molecule-1; vWF, von Willebrand factor; TGFbeta, Transforming growth factor beta; VEGF, vascular endothelial growth factor

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