Cilt Yaşlanması, Genetik Analizli Yaşlanma Karşıtı Tedavilerle Geri Döndürülebilir Mi?

Abstract

Cilt yaşlanması iç ve dış faktörlerden etkilenir. Stratum corneum keratinositlerden oluşur ve bunlar epidermisi olgunlaştırdıkça proliferatif potansiyelleri yavaş yavaş azalır ve cilt programlanmış yıkıma uğrar. Cilt yaşlanması ile ilişkili birçok tek nükleotid polimorfizm (SNP) vardır. COL1A1, MMP1 ve CYP1A2 genleri, kolajen yıkımı ve üretiminden sorumludur. Bu genlerdeki değişiklikler kolajen yıkımını ve üretimini etkiler. MCR1 ve STXBP5L genleri, ultraviyole (UV) koruması ve cildi nemlendirmek için önemlidir. Bu genlerdeki değişiklikler nedeniyle cilt UV ışınlarından iyi korunamaz ve cilt yaşlanması hızlanır. Derideki serbest radikaller arttıkça oksidatif stres artar. SOD2, GPX1 ve GSTP1 genleri vücudun oksidatif strese karşı korunmasında rol oynar. Ayrıca koenzim Q10 oksidatif strese karşı da etki eder. NQO1 genindeki değişiklik, koenzim Q10'u aktif formu olan ubiquinol'e dönüştüremez ve bu da ciltte oksidatif stresin artmasına neden olur. Cildin yaşlanmasını etkileyen bir diğer faktör de agresif bağışıklık sistemidir. TNF-α geni, bağışıklık sistemi tarafından üretilen inflamatuar yanıtları etkiler. TNF-α geni düzgün çalışmıyorsa, aşırı agresif bir reaksiyon oluşturabilir ve dokuya zarar verebilir. Ayrıca E Vitamini güçlü bir antioksidandır ve APOA5 genindeki değişiklikler E vitamini eksikliğine neden olur. Bu, cildin UV ışınlarından korunmasını etkiler. Cilt için bir diğer önemli vitamin ise C vitaminidir ve SLC23A1 geni C vitamini taşınmasında rol oynar. Bu gendeki değişiklikler C vitamini eksikliğine neden olur ve ciltte oksidatif stres ve kolajen üretimini etkiler. Bu polimorfizmler cildin yaşlanmasını etkileyen içsel ve dışsal faktörleri etkiler. Bireylerin cilt yaşlanmasının önüne geçebilmesi için bu polimorfizmlerin analiz edilmesi ve kişiye uygun cilt bakım ürünleri ile cilt yaşlanmasının geciktirilmesi sağlanabilir.

Keywords

• Cilt
• yaşlanma
• iç faktörler
• dış faktörler
• polimorfizmler

Can Skin Aging be Reversible by Anti-Aging Treatments with Genetic Analysis?

Abstract

Skin aging is affected by internal and external factors. The stratum corneum consists of keratinocytes, and as these mature in the epidermis, their proliferative potential gradually decreases and the skin undergoes programmed destruction. There are many single nucleotid polymorphism (SNP)s associated with skin aging. The COL1A1, MMP1, and CYP1A2 genes are responsible for collagen degradation and production. Changes in these genes affect collagen degradation and production. The MCR1 and STXBP5L genes are important for ultraviolet (UV) protection and moisturizing the skin. Due to changes in these genes, the skin cannot be well protected from UV rays, and skin aging accelerates. As free radicals in the skin increase, oxidative stress increases. The SOD2, GPX1, and GSTP1 genes play a role in protecting the body against oxidative stress. Also, coenzyme Q10 acts against oxidative stress. The change in the NQO1 gene cannot convert coenzyme Q10 to its active form, ubiquinol, which causes increased oxidative stress in the skin. Another factor that affects the aging of the skin is the aggressive immune system. The TNF-α gene influences the inflammatory responses generated by the immune system. If the TNF-α gene is not working properly, it can create an overly aggressive reaction and damage tissue. In addition, vitamin E is a powerful antioxidant, and changes in the APOA5 gene cause vitamin E deficiency. This affects the protection of the skin from UV rays. Another important vitamin for the skin is vitamin C, and the SLC23A1 gene is involved in vitamin C transport. Changes in this gene cause vitamin C deficiency and affect oxidative stress and collagen production in the skin. These polymorphisms affect the intrinsic and extrinsic factors that affect the aging of the skin. In order for individuals to prevent skin aging, these polymorphisms should be analyzed, and skin aging can be delayed with skin care products suitable for the person.

Keywords

• Skin
• aging
• internal factors
• external factors
• polymorphisms

References

1. 1. Pojšak B, Dahmane RG, Godic A. Intrinsic skin aging: The role of oxidative stress. Acta Dermatovenerologica. 2012;21(2):33-36. doi: 10.2478/v10162-012-0009-0.
2. 2. Kosmadaki MG, Gilchrest BA. The role of telomeres in skin aging/photoaging. Micron. 2004;35(3):155-159. doi: 10.1016/j.micron.2003.11.002.
3. 3. Yaar M, Gilchrest BA. Photoageing: mechanism, prevention and therapy. Br J Dermatol. 2007;157(5):874-887. doi: 10.1111/j.1365-2133.2007.08108.x.
4. 4. Tobin DJ. Introduction to skin aging. Journal of Tissue Viability. 2017;26(1):37-46. doi: 10.1016/j.jtv.2016.03.002.
5. 5. Kim JH, Ahn B, Choi SG, et al. Amino acids disrupt calcium-dependent adhesion of stratum corneum. PloS one. 2019;14(4):e0215244. doi: 10.1371/journal.pone.0215244.
6. 6. Ulucan K. Şampiyon Geni. İstanbul: Destek Yayınları; 2019:49-50.
7. 7. Mann V, Hobson EE, Li B, Stewart TL, Grant SF. A COL1A1 Sp1 binding site polymorphism predisposes to osteoporotic fracture by affecting bone density and quality. J Clin Invest. 2001;107(7):899-907. doi: 10.1172/JCI10347.
8. 8. Fujimoto T, Parry S, Urbanek M, et al. A single nucleotide polymorphism in the matrix metalloproteinase-1 (MMP-1) promoter influences amnion cell MMP-1 expression and risk for preterm premature rupture of the fetal membranes. J Biol Chem. 2002;277(8):6296-302. doi: 10.1074/jbc.M107865200.

9. 9. Rutter JL, Mitchell TI, Buttice G, et al. A single nucleotide polymorphism in the matrix metalloproteinase-1 promoter creates an Ets binding site and augments transcription. Cancer Res. 1998;58(23):5321–5325.
10. 10. Thorn CF, Aklillu E, McDonagh EM, Klein TE, Altman RB. PharmGKB summary: caffeine pathway. Pharmacogenet Genomics. 2012;22(5):389-395. doi: 10.1097/FPC.0b013e3283505d5e.
11. 11. Womack CJ, Saunders MJ, Bechtel MK, et al. The influence of a CYP1A2 polymorphism on the ergogenic effects of caffeine. J Int Soc Sports Nutr. 2012;9(1):7. doi: 10.1186/1550-2783-9-7.
12. 12. Rabe JH, Mamelak AJ, McElgunn PJ, Morison WL, Sauder DN. Photoaging: mechanisms and repair. J Am Acad Dermatol. 2006;55(1):1-19. doi: 10.1016/j.jaad.2005.05.010.
13. 13. Mumm CD, Draznin M. Melanocortin-1 receptor: loss of function mutations and skin cancer. Dermatol Online J. 2006;12(5):13.
14. 14. Elfakir A, Ezzedine K, Latreille J, et al. Functional MC1R-gene variants are associated with increased risk for severe photoaging of facial skin. J Invest Dermatol. 2010;130(4):1107-1115. doi: 10.1038/jid.2009.366.
15. 15. Le Clerc S, Taing L, Ezzedine K, et al. A genome-wide association study in caucasian women points out a putative role of the STXBP5L gene in facial photoaging. Journal of Investigative Dermatology. 2013;133(4):929-935. doi: 10.1038/jid.2012.458.
16. 16. Nobile V, Buonocore D, Michelotti A, Marzatico F. Anti-aging and filling efficacy of six types hyaluronic acid based dermo-cosmetic treatment: double blind, randomized clinical trial of efficacy and safety. J Cosmet Dermatol. 2014;13(4):277-287. doi: 10.1111/jocd.12120.
17. 17. Dai G, Freudenberger T, Zipper P, et al. Chronic ultraviolet B irradiation causes loss of hyaluronic acid from mouse dermis because of down-regulation of hyaluronic acid synthases. The American Journal of Pathology. 2007;171(5):1451–1461. doi: 10.2353/ajpath.2007.070136.
18. 18. Funke S, Risch A, Nieters A, et al. Genetic polymorphisms in genes related to oxidative Stress (GSTP1, GSTM1, GSTT1, CAT, MnSOD, MPO, eNOS) and Survival of rectal cancer patients after radiotherapy. Journal of Cancer Epidemiology. 2009;2009:6. doi: 10.1155/2009/302047.
19. 19. Mohammedi K, Patente TA, Bellili-Muñoz N, et al. Glutathione peroxidase-1 gene (GPX1) variants, oxidative stress and risk of kidney complications in people with type 1 diabetes. Metabolism. 2016;65(2):12-19. doi: 10.1016/j.metabol.2015.10.004.
20. 20. Sreeja L, Syamala V, Hariharan S, et al. Glutathione S-transferase M1, T1 and P1 polymorphisms: susceptibility and outcome in lung cancer patients. J Exp Ther Oncol. 2008;7(1):73-85.
21. 21. Lohan SB, Bauersachs S, Ahlberg S, et al. Ultra-small lipid nanoparticles promote the penetration of coenzyme 5 Q10 in skin cells and counteract oxidative stress. Eur J Pharm Biopharm. 2014;89:201-207. doi: 10.1016/j.ejpb.2014.12.008.
22. 22. Fischer A, Schmelzer C, Rimbach G, Niklowitz P, Menke T, Döring F. Association between genetic variants in the Coenzyme Q10 metabolism and Coenzyme Q10 status in humans. BMC Res Notes. 2011;4:245. doi: 10.1186/1756-0500-4-245.
23. 23. Hruza LL, Pentland AP. Mechanisms of UV-induced inflammation. J Invest Dermatol. 1993;100(1):35-41. doi: 10.1111/1523-1747.ep12355240.
24. 24. Lakka HM, Lakka TA, Rankinen T, et al. The TNF-α G-308A polymorphism is associated with C-reactive protein levels: The HERITAGE Family Study. Vascular Pharmacology. 2006;44(5):377–383. doi: 10.1016/j.vph.2006.02.002.
25. 25. Wu Y, Marvelle AF, Li J, et al. Genetic association with lipids in Filipinos: waist circumference modifies an APOA5 effect on triglyceride levels. Journal of lipid research. 2013;54(11):3198–3205. doi: 10.1194/jlr.P042077.
26. 26. Jiang CQ, Liu B, Cheung BM, et al. A single nucleotide polymorphism in APOA5 determines triglyceride levels in Hong Kong and Guangzhou Chinese. Eur J Hum Genet. 2010;18(11):1255-60. doi: 10.1038/ejhg.2010.93.
27. 27. Wilson JX. Regulation of vitamin C transport. Annual Review of Nutrition. 2005;25(1):105-125. doi: 10.1146/annurev.nutr.25.050304.092647.
28. 28. Timpson NJ, Forouhi NG, Brion MJ, et al. Genetic variation at the SLC23A1 locus is associated with circulating concentrations of L-ascorbic acid (vitamin C): evidence from 5 independent studies with>15,000 participants. The American Journal of Clinical Nutrition. 2010;92(2):375–382. doi: 10.3945/ajcn.2010.29438.