Total Defense + Repair: A Novel Concept in Solar Protection and Skin Rejuvenation

However, this last decade has seen the development of a growing body of evidence indicating that infrared (IR) radiation and visible light are also responsible for changes in the skin physiology that can lead to premature aging, pigmentary changes, or other pathologies in human skin.^6,7,8

The appearance of skin reflects a combination of one’s general health, ethnicity, life style, diet, and age. These features determine the color, texture, firmness, and smoothness of the skin. Intrinsic aging is a naturally-occurring process that relates closely to chronological age. At a microscopic level, chronologically- aged skin can be characterized by an atrophic epidermis with flattening of the dermal-epidermal junction and loss of the Rete pegs,⁹ as well as a decrease in the number of fibroblasts and collagen, resulting in a much thinner dermis than that observed in young individuals.¹⁰

The skin is the only organ chronically exposed to the environment, and the resulting interaction with environmental factors can strongly influence skin physiology, leading to extrinsic aging. By far the most studied source of extrinsic skin damage is solar radiation.^4,11,12

The term “photoaging” was first coined in 1986 in an attempt to describe the effect of chronic UV-light exposure on the skin.¹³ It has been estimated that photoaging accounts for up to 90% of visible skin extrinsic aging. Photoaged skin is characterized by dryness, a rough texture, increased skin laxity, irregular pigmentation, telangiectasia (or angioectasias), a yellowish color, plaque-like thickening, deep creases, and fine wrinkles.^11,14 Solar elastosis is the dermal hallmark of photoaged skin.^15,16 In addition, photodamaged skin also presents an extensive decrease of fibrillar collagen (types I and III)^17-20 due to the decrease in transforming growth factor (TGF)-β levels and the activation of activator protein-1 (AP-1).^10,21,22 Changes in the extracellular matrix (ECM) composition result in decreased mechanical tension on the cell surface of fibroblasts, triggering cellular collapse that aggravates the already diminished collagen synthesis and increases MMPs expression even further. On the other hand, a photoaged epidermis shows hyperplasia or atrophy, as well as the disappearance of dermal papillae, thickness of the basement membrane, an increased number of melanocytes and melanomes, presence of atypical keratinocytes, parakeratosis, and thickness of the stratum corneum.^23,24

Previously, the negative effects of solar light on human skin were primarily attributed to wavelengths in the UVB and UVA range.^25-28 However, recent research has shown that other solar wavelengths, such as IR and visible light, may also play a key role in extrinsic skin aging. Human skin is predominantly exposed to IR radiation, which accounts for 54.3% of total solar light.⁶

Infrared radiation is comprised of IR-A (760 nm - 1,400 nm), IR-B (1,400 nm - 3,000 nm), and IR-C (3,000 nm - 1 x 106 nm). Among them, IR-A accounts for 30% of total solar radiation and has the capacity to penetrate deeper into the skin, reaching subcutaneous tissues (Figure 1). Nowadays, there is compelling evidence that associates solar IR-A radiation with premature aging and the progression of malignancies.^1,29-31 Interestingly, for many years IR-light based therapies have been used clinically to promote wound healing, protect muscles from stress, and reduce proinflammatory cytokine and chemokine production.6 The apparent dichotomy of IR-A and its effect on the skin (good or bad? friend or foe?) is explained by the capacity to control the intensity, time of exposure, and heat production during clinical exposure to IR-A.³²

IR-A regulates proximally 600 genes in human skin that are involved in ECM homeostasis, apoptosis, cell growth, and stress responses.^8,30,33,34 While the mechanisms by which this occurs are highly complex, it is thought that many of the pathological effects of IR-A are attributable to the altered function of mitochondria, as the cytochrome c oxidase from complex IV acts as its photo-acceptor.^1,35 Interestingly, it has been shown that simultaneous exposures to multiple wavelength of low energy light (ie, visible and near IR radiations) also modulated cell metabolism and gene expression, indicating that ratios of different solar rations may impact skin premature aging.³⁶ IR-A–induced mitochondrial changes (ie, increase in mitochondrial reactive oxygen species [ROS] production, decreased adenosine triphosphate [ATP] synthesis, and enhanced permeability) are responsible for the activation of a retrograde signaling pathway that can trigger activation of mitogen-activated protein kinases (MAPKs) and caspases (apoptosis). ³⁵ MAPK pathways play a critical role in controlling the expression of MMP-1 and therefore ECM destruction.^1,6,37 Moreover, studies using different experimental models showed that IR radiation enhanced the deposit of elastotic material in the dermis while decreasing collagen. Epidermal hyperplasia/thickening, increased senescent marker expression (ie, telomerase expression and activity), angiogenesis (by increasing vascular endothelial growth factor [VEGF] production and CD31 positive cells), erythema, and swelling are also characteristics present in IR-radiated skin. Finally, IR-A also triggers a significant decrease in antioxidant capacity in the skin (specifically by destroying carotenoids such as β-carotenes and lycopene), as well as the activation-recruited mast cells (MC_TC), enhance oxidative stress and inflammation, promoting premature aging.^38-40