So the question rises, is visible light friend or foe? The answer most probably lies somewhere in between. Importantly, although visible light constitutes a substantial part of the solar spectrum, the strength of its physiological effects should be placed into context with that of UV radiation. For instance, UV was reported to be 25 times more efficient at inducing pigmentation in people with darker skin, compared to visible light 29 . Moreover, although visible light can affect DNA structure, a study performed on Chinese hamster cells suggested that it contributes to less than 10% of total DNA damage caused by solar exposure 26 . Finally, even though visible light has measurable effects on signalling pathways known to precipitate skin ageing, its significance in the process of photoageing still needs to be clarified.

For instance, similar to what is seen with UVA, irradiation of skin with visible light was reported to generate ROS following photon‐induced activation of endogenous photosensitizers 21 , 22 . To quantify the relative contribution of UVB, UVA and visible light to ROS generation, ex vivo skin explants were exposed to natural midday sunlight in the presence of a set of filters. Results estimated the generation of ROS at 4% for UVB, 46% for UVA and 50% for visible light 21 . Visible light skin chromophores include haemoglobin, melanin, bilirubin, riboflavin and porphyrins 23 . At doses equivalent to 15–90 min of sunlight exposure, visible light also induces inflammatory cytokines (IL‐1, IL‐6, IL‐8, GM‐CSF,) and increases the expression of matrix degrading enzymes (MMP‐1 and MMP‐9) in human epidermal equivalents , whereas free radical production was confirmed in vivo using chemiluminescence and skin biopsies 22 , 24 . Visible light additionally appears to affect DNA through the formation of oxidized DNA bases as seen with UVA 25 , 26 , but not through dimer formation 22 . Finally, visible light induces pigment darkening in subjects with darker skin (Fitzpatrick type IV–V) 27 and is suspected of being an aggravating factor in melasma 28 .

Of even lesser energy, visible light (400–700 nm) accounts for approximately 50% of the total solar spectrum 11 . It penetrates deeply into biological tissues and about 20% reaches the hypodermis 11 . We enjoy visible light; it allows us to see the world, helps plants to grow providing us with food and oxygen, is useful in treating certain skin conditions, and certainly seems inoffensive. But is it really? Very few studies have addressed the question so far, but their results revealed that visible light affects skin physiology in many ways and this is already changing the way we are looking at light.

Infrared radiation

IR has the lowest energy. However, its contribution to the solar spectrum reaching human skin is around 45%. IR comprises IRA (700–1400 nm), IRB (1400–3000 nm) and IRC (3000 nm–1 mm). IRB and IRC do not penetrate the skin very deeply, but IRA does. IRA represents about 30% of IR radiation, of which 65% reaches the dermis and 10% the hypodermis 11. As is the case with UV and visible light, IRA generates ROS within the skin. The relative contribution of IRA to free radicals generation, in Berlin summer midday sunlight, has been estimated to be around one‐fourth of that of UV 21. IRA also induces unbalanced gene expression of MMP and decreases collagen gene expression in vitro and in vivo, favours angiogenesis, is involved in photoageing, may promote carcinogenesis and, additionally, affects mitochondrial integrity 21, 24, 30-32. However, unlike UV and visible light, IR is poorly absorbed by usual skin chromophores, such as melanin, and is too weak to directly affect DNA. So how are all these effects occurring?

The skin response to IR type A (IRA) radiation has been proposed recently to involve mitochondria with cytochrome C oxidase (CcO) as a potential chromophore 31, 33. Interaction of IRA with CcO could lead to disruption of the mitochondrial electron transport chain, resulting in inadequate energy production and increased generation of ROS. Such mitochondrial dysfunctions are known to trigger retrograde mitochondrial signalling from mitochondria to the cell nucleus, commanding expression of specific nuclear genes 34. In fibroblasts, gene regulatory effects are observed at IRA dosage of 54–360 J/cm2 and ROS production can be detected even at IRA intensity levels as low as 30 J/cm2 35; considering that a dosage of 300–800 J/cm2 can easily be reached under the sun, in a summer day in central Europe, these experimental dosages can be considered as physiologically relevant 36.

Retrograde mitochondrial signalling is a survival pathway of communication that operates through ERK1/2 activation and elevation of free Ca2+ in the cytosol of cells. In skin, the pathway culminates in the modulation of genes involved in photoageing, including MMP‐1 and type 1 procollagen (COL1A1) (Fig. 3) 31-33. The combination of stimulated collagen degradation and reduced collagen renewal generated by increased MMP and lesser COL1A1 expression, respectively, is recognized to significantly contribute to the formation of wrinkles in photoageing 37. However, when tested in vivo, the magnitude of IRA‐induced MMP‐1 upregulation in skin showed considerable interindividual variability and up to 20% of the volunteers had no response at all 38. The reason for such discrepancies remains unclear, but does not appear to be related to skin type 38. However, as IRA‐induced ROS production (at the basis of retrograde signalling) has been linked to skin temperature 21, one possible explanation may come from differences in IRA‐induced changes in this parameter among the participants.

Figure 3 Open in figure viewer PowerPoint 31-33 Infrared A‐induced retrograde signalling Infrared type A (IRA) radiation leads to a burst of mitochondrial reactive oxygen species (ROS), which in turn initiates retrograde signalling, from mitochondria to nucleus, where it alters expression of genes involved in skin ageing, such as matrix metalloproteinase‐1 (MMP‐1) and procollagen alpha‐1 (COL1A1). The combination of stimulated collagen degradation and reduced collagen renewal generated by increased MMP and lesser COL1A1 expression, respectively, contributes to the formation of wrinkles in photoageing.

Indeed, part of the answer of skin to IR radiation may lie in the fact that IR light has the particularity of interacting with molecules within tissues, generating molecular vibrations that produce heat 11. This is the cause of the warmth sensation that we feel when exposing ourselves to sunlight. IRB and IRC are mainly responsible for the generation of heat in skin. Keratinocytes, fibroblasts and melanocytes express various thermo‐sensitive receptors at their membrane, including the transient receptor potential vanilloid 1 (TRPV1), which was recently proposed to be activated by IR radiation, in addition to temperature >43 °C, low pH and capsaicin 39. TRPV1 is a cell membrane channel that opens upon stimulation, allowing a flux of calcium ions to cross the membrane and rush into cell.

In skin, prolonged heat activation is associated with inflammation, elastosis and dermal collagen breakdown in vitro and in vivo 40, 41. Chronic IR exposure has similar effects that may be mediated, at least partly, through the generation of heat 42. The proposed mechanism involves heat‐induced and protein kinase C (PKC)‐potentiated activation of TRPV1 at the membrane of skin cells, allowing calcium ions inside (Fig. 4). In fibroblasts, TRPV1 activation induces MMP‐1 expression, at the mRNA and protein levels, resulting in increase in collagen degradation and premature skin ageing 30, 41. In cutaneous sensory neuronal cells, TRPV1 activation stimulates the release of neuropeptides, such as substance P (SP), which increases vasodilatation and vascular permeability in skin, through the promotion of VEGF secretion by mast cells 43. Synergistic activation of TRPV1 on both skin cells may result in inflammation and precipitate skin ageing even further. Interestingly, TRPV1 expression is increased in old skin suggesting a link with pruritus, a common complaint in elderly people 41, 44.

Figure 4 Open in figure viewer PowerPoint 40, 41 43 44 Activation of the TRPV1 ion channel by IR and heat in skin in keratinocytes, transient receptor potential vanilloid 1 (TRPV1) activation by infrared radiation (IR) and heat promotes calcium influx and induces matrix metalloproteinase‐1 (MMP‐1) expression, resulting in collagen degradation. On skin sensory nerve fibres, TRPV1 activation stimulates the release of substance P (SP), which mediates vasodilatation and vascular permeability, through the promotion of vascular endothelial growth factor (VEGF) secretion by mast cell. Synergistic activation of TRPV1 on both skin cells favours inflammation and precipitates skin ageing. Expression of TRPV1 is increased in aged skin

Thus, IR exposure appears to have non‐negligible effects on skin physiology that are mediated through various molecular mechanisms. However, we still do not know which one is most important and to what extent these mechanisms, globally and individually, contribute to skin changes with ageing. As is the case for visible light, the biological relevance of IR effects in relation to UV needs to be clarified.