Elastic fibres are essential extracellular matrix macromolecules comprising an elastin core surrounded by a mantle of fibrillin-rich microfibrils. They endow connective tissues such as blood vessels, lungs and skin with the critical properties of elasticity and resilience. The biology of elastic fibres is complex because they have multiple components, a tightly regulated developmental deposition, a multi-step hierarchical assembly and unique biomechanical functions. However, their molecular complexity is at last being unravelled by progress in identifying interactions between component molecules, ultrastructural analyses and studies of informative mouse models.

The quality of life of ageing populations is increasingly determined by age-related changes to the mechanical properties of numerous biological tissues. Degradation and mechanical failure of these tissues has a profound effect on human morbidity and mortality. Soft tissues have complex and intricate structures and, similar to engineering materials, their mechanical properties are controlled by their microstructure. Thus age-relate changes in mechanical behavior are determined by changes in the properties and relative quantities of microstructural tissue components. This review focuses on the cardiovascular system; it discusses the techniques used both in vivo and ex vivo to determine the age-related changes in the mechanical properties of arteries.

The ability of elastic tissues to deform under physiological forces and to subsequently release stored energy to drive passive recoil is vital to the function of many dynamic tissues. Within vertebrates, elastic fibres allow arteries and lungs to expand and contract, thus controlling variations in blood pressure and returning the pulmonary system to a resting state. Elastic fibres are composite structures composed of a cross-linked elastin core and an outer layer of fibrillin microfibrils. These two components perform distinct roles; elastin stores energy and drives passive recoil, whilst fibrillin microfibrils direct elastogenesis, mediate cell signalling, maintain tissue homeostasis via TGFβ sequestration and potentially act to reinforce the elastic fibre. In many tissues reduced elasticity, as a result of compromised elastic fibre function, becomes increasingly prevalent with age and contributes significantly to the burden of human morbidity and mortality. This review considers how the unique molecular structure, tissue distribution and longevity of elastic fibres pre-disposes these abundant extracellular matrix structures to the accumulation of damage in ageing dermal, pulmonary and vascular tissues. As compromised elasticity is a common feature of ageing dynamic tissues, the development of strategies to prevent, limit or reverse this loss of function will play a key role in reducing age-related morbidity and mortality.

Synopsis: Cutaneous ageing is the result of two distinct, biological processes which may occur concurrently: (i) the passage of time, termed intrinsic ageing and (ii) environmental influences, termed extrinsic ageing. Intrinsic ageing of the skin is a slow process which causes changes in tissue structure and impairs function in the absence of additional biological, chemical and physical factors. The clinical features of intrinsically aged skin are not usually evident until old age when, although smooth and unblemished, the skin surface appears pale and is characterized by fine wrinkles with occasional exaggerated expression lines. Functionally, intrinsically aged skin is dry and less elastic than more youthful skin. In contrast, extrinsically aged skin is exemplified by deep, coarse wrinkles, mottled hyperpigmentation and a marked loss of elasticity and recoil. The two major environmental influences which induce extrinsic ageing are: (i) chronic exposure to solar ultraviolet (UV) irradiation (termed photoageing) and (ii) smoking. This review discusses the changes associated with the ageing process in the skin, with particular emphasis on the role played by the elastic fibre network in maintaining dermal function. The review concludes with a discussion of a short‐term assay for independent assessment of the efficacy of anti‐ageing cosmetic products using the elastic fibre component fibrillin‐1 as a biomarker of extracellular matrix repair.