The latest issue of the Journal of Investigative Dematology Symposium Proceedings includes a set of papers theorizing on the mechanisms by which exposure to sunlight accelerates the characteristic ways in which skin changes with age. In many ways its a good illustration of just how far there is to go in pulling together present knowledge of aging biochemistry into theories that are both unifying and specific: the researchers here argue on mechanisms from a number of quite different and distinct viewpoints.
Some of the papers are presently free to read, so take a look while that lasts.
UV-induced melanogenesis (tanning) and "premature aging" or photoaging result in large part from DNA damage. This article reviews data tying both phenomena to telomere-based DNA damage signaling and develops a conceptual framework in which both responses may be understood as cancer-avoidance protective mechanisms.
The exact pathogenesis of photoaging of the skin is not yet known. Earlier, a number of molecular pathways explaining one or more characteristics of photoaged skin have been described, but a unifying mechanistic concept is still missing. Here we propose the "Defective Powerhouse Model of Premature Skin Aging", which reconciles most of the earlier conducted research as one concept. In this model, the persistence of UV radiation-induced mtDNA deletions or the infrared radiation-induced disturbance of the electron flow of the mitochondrial electron transport chain leads to inadequate energy production in dermal fibroblasts. As a consequence of this defective powerhouse, retrograde mitochondrial signaling pathways are triggered that then they transduce functional and structural alterations in the skin.
UV radiation from the sun impacts skin health adversely through complex, multiple molecular pathways. Premature skin aging (photoaging) is among the most widely appreciated harmful effects of chronic exposure to solar UV radiation. Extensive damage to the dermal connective tissue is a hallmark of photoaged skin. Disruption of the normal architecture of skin connective tissue impairs skin function and causes it to look aged. UV irradiation induces expression of certain members of the matrix metalloproteinase (MMP) family, which degrade collagen and other extracellular matrix proteins that comprise the dermal connective tissue. Although the critical role of MMPs in photoaging is undeniable, important questions remain.
Researchers are largely on the same page when it comes to how aged skin is different from young skin - questions revolve around the processes that lead to that point. As for aging research in general, you can see camps in any sub-field - such as skin aging here - emerge and center around known areas of interest such as mitochondrial damage, telomere shorting, or nuclear DNA damage.
As in other parts of aging research, no great resolution has been reached as to how much each of these processes contribute to overall degeneration, and which processes might be cause or effect of other processes. All sides have indirect evidence to point to in support of their position, so this might continue for another decade before an evidence-backed consensus emerges.
Krutmann, J., & Schroeder, P. (2009). Role of Mitochondria in Photoaging of Human Skin: The Defective Powerhouse Model Journal of Investigative Dermatology Symposium Proceedings, 14 (1), 44-49 DOI: 10.1038/jidsymp.2009.1