Protecting telomeres to ensure longevity

Today, it seems that different factors are interlinked and combined with other processes and on different levels to contribute to the skin ageing phenomenon. On a cell level, telomeres’ shortening is considered one of the main characteristics of ageing.

Over the course of cell divisions, the telomeres gradually shorten until they reach a critical minimum size, triggering cell senescence which contributes to the degeneration of the skin tissue and its ageing. In skin cells, telomeres are stabilised by a multiprotein complex, called telosome or shelterin. In the absence of the telosome, the weakened telomeres shorten more quickly at each division. Stress (UV, reactive oxygen species, etc.) also accentuates their wear. This leads to gradual depletion of the cell and its premature ageing. In this article, we discuss the in vitro models we developed for studying the capacity of a natural active ingredient to limit deterioration of the telosome. This active prevents the accelerated erosion of telomeres induced by stress and slows down premature passage of skin cells into the senescent phase and thus ensures longevity. This new anti-ageing strategy is supported by proven cosmetic benefits: the marks of ageing on the skin are reduced and the perceived age is improved.

One of the first visible consequences of ageing is the modification of skin parameters, characterised by the development of wrinkles and sagging of the skin. On a cell level, ageing is known as senescence, an irreversible state in which the damaged cells no longer proliferate. There are two major types of senescence: premature senescence triggered by stress and replicative senescence. The latter is inherent to cell division and indicates a decline in the replicative potential of fibroblasts. In fact, cells have a division quota (around 60 for fibroblasts), which determines their life span. Once this quota is used up, the fibroblasts stop proliferating and enter the senescence phase, a normal physiological process that prevents transformation of the cell. This is the Hayflick limit or replicative senescence. This countdown is dictated by telomeres, non-encoding, highly repeated DNA sequences located at the extremities of the chromosomes. Over the course of cell divisions, the telomeres gradually shorten until they reach a critical minimum size, triggering cell senescence. This is characterised by the cessation of proliferation, a flattened morphology of the cell and the expression of -galactosidase, contributing to the degeneration of the skin tissue and its ageing.1,2 Telomeres ensure the integrity of chromosomes. Firstly, they protect the ends of the chromosomes, like a shoelace tip, preventing them from fraying, and, secondly, they prevent the loss of genetic information during replication. But these chromosome ends are fragile and are themselves stabilised by a multiprotein complex, called telosome or shelterin complex (Fig. 1).

The telosome: the protective cap of telomeres

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