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Cited by 151Dermatology and Skin DiseasesAcne and Rosacea Treatments and EffectsLipid metabolism and biosynthesis

Sebaceous-immunobiology is orchestrated by sebum lipids

Open access
Lovászi, Marianna, Szegedi, Andrea, Zouboulis, Christos C., Törőcsik, Dániel·2017·Dermato-Endocrinology
DOI 10.1080/19381980.2017.1375636PMC PMC5821166
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Abstract

The major role of sebaceous glands in mammals is to produce sebum, which coats the epidermis and the hair providing waterproofing, thermoregulation and photoprotection. However, as the need for these functions decreased along the evolutionary changes in humans, a relevant question has been raised: are sebaceous glands and sebum the remnants of our mammalian heritage or do they have overtaken a far more complex role in human skin biology? Trying to provide answers to this question, this review introduces the evolving field of sebaceous immunobiology and puts into the focus the pathways that sebum lipids use to influence the immune milieu of the skin. By introducing possible modifiers of sebaceous lipogenesis and discussing the - human-specific - alterations in composition and amount of sebum, the attribute of sebum as a sensitive tool, which is capable of translating multiple signalling pathways into the dermal micro environment is presented. Further their interaction with macrophages and keratinocytes involves sebum lipid fractions into disease pathogenesis, which could lead - on the other side - to the development of novel sebum-based therapeutic strategies.

AI snapshot

Written from the paper’s full text.

TL;DR

This review argues that sebum lipids are not merely passive barrier components but active orchestrators of sebaceous-immunobiology, shaping skin immune responses and disease pathogenesis. It synthesizes evidence that sebum composition is altered in acne, seborrheic dermatitis, rosacea, psoriasis, and atopic dermatitis, and that sebum lipids modulate macrophages, keratinocytes, and the microbiome.

Key findings

  • Human sebum is dominated by triglycerides/fatty acids (57.5% of total lipids), wax esters (26%), squalene (12%), and cholesterol (4.5%); unique sebaceous fatty acids include sapienic acid (C16:1Δ6) and sebaleic acid (18:2Δ5,8), with sapienic and oleic acid showing strong antibacterial/anti-inflammatory properties.
  • Ex vivo Raman spectroscopy showed topically applied linoleic, stearic, oleic, palmitic acids and squalene penetrate epidermis into dermis; Oil Red staining revealed diffuse lipid accumulation in upper dermis of sebaceous gland-rich vs -poor skin.
  • Sebum lipids modulate immune cells: linoleic and oleic acid induce alternative macrophage activation and enhance phagocytosis of particles and *P. acnes*; linoleic acid increases keratinocyte TSLP mRNA dose-dependently, and sebocyte supernatant increases TSLP.
  • Disease-associated sebum alterations include acne (elevated sebum, altered saturated/unsaturated ratio, increased C16:0/C16:1 ratio improves acne, decreased linoleic acid, squalene peroxide/PPAR activation), rosacea (elevated myristic acid C14:0, reduced saturated long-chain fatty acids), seborrheic dermatitis (*Malassezia* lipases increase FFA), psoriasis (sebaceous atrophy without significant total sebum change), and AD (severely reduced sebum production).

Methods

  • Narrative review; no systematic search or meta-analysis described.
  • Synthesizes published literature and the authors’ prior studies, including an ex vivo Raman spectroscopy penetration study, Oil Red staining, macrophage/keratinocyte experiments, and one mention of own unpublished AD data.
  • Main analysis is thematic: sebum lipid composition, dermal penetration, disease-associated alterations, immune functions, signaling pathways, and therapeutic perspectives.

Limitations

  • Stated: exact mechanisms linking altered sebaceous gland function to AD remain unelucidated; it is still unknown how sebum lipids contribute to the skin inflammatory milieu; further research in sebocyte function and lipidomics is required.
  • Evident: as a narrative review, it lacks systematic search, quality appraisal, or quantitative synthesis; some claims rely on the authors’ own unpublished data; no primary experimental data are reported in this paper.

Model-written summary. Check it against the paper before relying on it.

Integrity signals

Registry

Crossref · 10.1080/19381980.2017.1375636

Cites

93 of 93 references verified0 citation errors · 0 not checkable

Statistics

Nothing to recompute.

Claims the paper makes

55 of 129 cited sources checked · 21 supported · 3 flagged · accuracy not yet measured

  • Premisecitation

    Stearoyl-CoA Δ-6 desaturase induces rapid oxidation and degradation of linoleic acid and its derivatives in sebaceous gland cells.

    “Ge et al. identified stearoyl-CoA Δ-6 desaturase as the major fatty acid desaturase in human sebaceous glands, which induces rapid oxidation and degradation of linoleic acid and its derivatives in sebaceous gland cells.11”
    Quote in the paperNot a substantial claim1 of 1 sources checked
    • cites [11] Ge L, Gordon JS, Hsuan C, Stenn K, Prouty SM Identification of the delta-6 desaturase of human sebaceous glands: expression and enzyme activity. J Invest Dermatol. 2003; 120: 707– 14. doi: 10.1046/j.1523-1747.2003.12123.x. PMID:12713571. 12713571 source

      The Abstract (page unavailable) identifies Δ-6 desaturase/FADS2 as the major fatty acid desaturase in human sebaceous glands. The Discussion (page unavailable) instead suggests that linoleate catabolism may involve 15-lipoxygenase-2 and shield FADS2 from linoleate; it does not say FADS2 induces rapid oxidation or degradation of linoleic acid or its derivatives. The paper calls the enzyme FADS2, not stearoyl-CoA desaturase. (LLM, conf=0.90)

      Experimental — accuracy not yet measured
  • Premisecitation

    Squalene neutralizes the formation of UV irradiation-induced reactive oxygen species in the skin.

    “Due to its prominent lubricant and penetration efficiency squalene is capable of neutralizing the formation of UV irradiation-induced reactive oxygen species in the skin.6,7”
    Quote in the paperNot a substantial claim1 of 2 sources checked
    • cites [6] Ohsawa K, Watanabe T, Matsukawa R, Yoshimura Y, Imaeda K The possible role of squalene and its peroxide of the sebum in the occurrence of sunburn and protection from the damage caused by U.V. irradiation. J Toxicol Sci. 1984; 9: 151– 9. doi: 10.2131/jts.9.151. PMID:6481825. 6481825 source

      The Discussion (p. 8) proposes that squalene protects the skin surface by trapping UV energy through peroxidation. It does not say that squalene neutralizes the formation of reactive oxygen species; the Results (p. 4) instead report increased squalene oxidation after UV irradiation. The cited paper also does not attribute this effect to lubricant or penetration efficiency. (LLM, conf=0.84)

      Experimental — accuracy not yet measured
    • cites [7] Picardo M, Zompetta C, De Luca C, Cirone M, Faggioni A, Nazzaro-Porro M, Passi S, Prota G Role of skin surface lipids in UV-induced epidermal cell changes. Arch Dermatol Res. 1991; 283: 191– 7. doi: 10.1007/BF00372061. PMID:1867482. 1867482 source
  • Premisecitation

    Acne patients have a markedly altered sebum composition.

    “In the recent years numerous studies have showed, that in addition to an elevated sebum production, acne patients have a markedly altered sebum composition.24,25”
    Quote in the paperSubstantial claim1 of 2 sources checked
    • cites [24] Ottaviani M, Camera E, Picardo M Lipid mediators in acne. Mediators of inflammation. 2010; 2010. doi: 10.1155/2010/858176. PMID: 20871834 20871834 PMC2943135 source
    • cites [25] Zouboulis CC, Jourdan E, Picardo M Acne is an inflammatory disease and alterations of sebum composition initiate acne lesions. J Eur Acad Dermatol Venereol. 2014; 28: 527– 32. doi: 10.1111/jdv.12298. PMID:24134468. 24134468 source
  • Premisecitation

    Acne patients have elevated sebum production.

    “In the recent years numerous studies have showed, that in addition to an elevated sebum production, acne patients have a markedly altered sebum composition.24,25”
    Quote in the paperNot a substantial claim1 of 2 sources checked
    • cites [24] Ottaviani M, Camera E, Picardo M Lipid mediators in acne. Mediators of inflammation. 2010; 2010. doi: 10.1155/2010/858176. PMID: 20871834 20871834 PMC2943135 source
    • cites [25] Zouboulis CC, Jourdan E, Picardo M Acne is an inflammatory disease and alterations of sebum composition initiate acne lesions. J Eur Acad Dermatol Venereol. 2014; 28: 527– 32. doi: 10.1111/jdv.12298. PMID:24134468. 24134468 source
  • Premisecitation

    Stearoyl-CoA Δ-6 desaturase is the major fatty acid desaturase in human sebaceous glands.

    “Ge et al. identified stearoyl-CoA Δ-6 desaturase as the major fatty acid desaturase in human sebaceous glands, which induces rapid oxidation and degradation of linoleic acid and its derivatives in sebaceous gland cells.11”
    Quote in the paperNot a substantial claim1 of 1 sources checked
    • cites [11] Ge L, Gordon JS, Hsuan C, Stenn K, Prouty SM Identification of the delta-6 desaturase of human sebaceous glands: expression and enzyme activity. J Invest Dermatol. 2003; 120: 707– 14. doi: 10.1046/j.1523-1747.2003.12123.x. PMID:12713571. 12713571 source

      The Abstract (page not provided) identifies Δ-6 desaturase/FADS2 as the major fatty acid desaturase in human sebaceous glands. But the Discussion (page not provided) distinguishes it from stearoyl-CoA desaturase (SCD), reporting very low SCD expression in those glands; the claim conflates the two enzymes. (LLM, conf=0.88)

      Experimental — accuracy not yet measured
  • May combine two claims. 31
  • Classified as probably not a substantial claim. 8

  • May combine two claims.

    Premisecitation

    Accumulation of lipid peroxides, specifically squalene peroxide, activates PPARs, stimulates keratinocyte proliferation and lipoxygenase activity, and overall increases the expression and secretion of proinflammatory cytokines in acne.

    “Another interesting aspect of the detected changes is the accumulation of lipid peroxides, specifically squalene peroxide, which activates the Peroxisome Proliferator Activated Receptors (PPARs), stimulate keratinocyte proliferation and lipoxygenase (LOX) activity, overall increasing the expression and secretion of proinflammatory cytokines in acne.27-29”
    Quote in the paperSubstantial claim1 of 3 sources checked
    • cites [27] Jeremy AH, Holland DB, Roberts SG, Thomson KF, Cunliffe WJ Inflammatory events are involved in acne lesion initiation. J Invest Dermatol. 2003; 121: 20– 7. doi: 10.1046/j.1523-1747.2003.12321.x. PMID:12839559. 12839559 source
    • cites [28] Zouboulis CC Is acne vulgaris a genuine inflammatory disease? Dermatology (Basel, Switzerland). 2001; 203: 277– 9. doi: 10.1159/000051771. PMID:11752811. 11752811 source
    • cites [29] Delerive P, Fruchart JC, Staels B Peroxisome proliferator-activated receptors in inflammation control. The Journal of endocrinology. 2001; 169: 453– 9. doi: 10.1677/joe.0.1690453. PMID:11375115. 11375115 source

      The Abstract (page unavailable) says PPAR activators inhibit expression of proinflammatory genes, including cytokines. “Is there a role for PPAR in inflammation?” (page unavailable) likewise reports inhibition of several cytokines, contrary to the claimed overall increase. The cited paper does not address squalene peroxide, keratinocyte proliferation, or acne. (LLM, conf=0.87)

      Checked by a reasoning model — may be wrong.

      Experimental — accuracy not yet measured

  • May combine two claims.

    Premisecitation

    An increase in the C16:0/C16:1 nutrition lipid ratio has been shown to improve acne, accompanied by diminishing levels of linoleic acid content.

    “An altered ratio between saturated and unsaturated fatty acids has been identified, and particularly, an increase in the C16:0/C16:1 nutrition lipid ratio has been shown to improve acne, accompanied by diminishing levels of linoleic acid content.24,26”
    Quote in the paperNot a substantial claim1 of 2 sources checked
    • cites [24] Ottaviani M, Camera E, Picardo M Lipid mediators in acne. Mediators of inflammation. 2010; 2010. doi: 10.1155/2010/858176. PMID: 20871834 20871834 PMC2943135 source

      Section 3.2 reports that the C16:0/C16:1 ratio in skin-surface lipids is higher in acne, not that increasing it improves acne. Section 3.1 likewise describes diminished linoleic acid in affected patients and links low levels to processes involved in comedone formation. (LLM, conf=0.88)

      Checked by a reasoning model — may be wrong.

      Experimental — accuracy not yet measured
    • cites [26] Smith RN, Braue A, Varigos GA, Mann NJ The effect of a low glycemic load diet on acne vulgaris and the fatty acid composition of skin surface triglycerides. J Dermatol Sci. 2008; 50: 41– 52. doi: 10.1016/j.jdermsci.2007.11.005. PMID:18178063. 18178063 source

  • May combine two claims.

    Premisecitation

    An increase in the levels of phospholipids, triacylglycerols, and cholesterol was found in the epidermis of psoriatic patients, which correlated with the severity of psoriasis.

    “However, an increase in the levels of phospholipids, triacylglycerols, and cholesterol were found in the epidermis of psoriatic patients, which correlated with the severity of psoriasis.36–38”
    Quote in the paperNot a substantial claim1 of 3 sources checked
    • cites [36] Liakou AI, Nyengaard JR, Bonovas S, Knolle J, Makrantonaki E, Zouboulis CC Marked Reduction of the Number and Individual Volume of Sebaceous Glands in Psoriatic Lesions. Dermatology (Basel, Switzerland). 2016; 232: 415– 24. doi: 10.1159/000445942. PMID:27250651. 27250651 source
    • cites [37] Rittie L, Tejasvi T, Harms PW, Xing X, Nair RP, Gudjonsson JE, Swindell WR, Elder JT Sebaceous Gland Atrophy in Psoriasis: An Explanation for Psoriatic Alopecia? J Invest Dermatol. 2016; 136: 1792– 800. doi: 10.1016/j.jid.2016.05.113. PMID:27312025. 27312025 PMC5112032 source

      The Results report no apparent difference in neutral-lipid staining of the stratum corneum between lesional and nonlesional skin. The Discussion likewise reports no obvious stratum-corneum staining difference and markedly reduced staining in sebaceous glands, rather than the claimed lipid increase. The paper does not report a correlation of epidermal lipid levels with psoriasis severity. (LLM, conf=0.78)

      Checked by a reasoning model — may be wrong.

      Experimental — accuracy not yet measured
    • cites [38] Tsambaos D, Kalofoutis A, Stratigos J, Miras C, Capetanakis J Thin-layer chromatography of phospholipid components of normal and psoriatic epidermis. Br J Dermatol. 1977; 97: 135– 8. doi: 10.1111/j.1365-2133.1977.tb15058.x. PMID:911675. 911675 source

  • May combine two claims.

    Premisecitation

    Oleic acid (18:1Δ9), a major ω9 monounsaturated fatty acid of sebum triglycerides, exerts the strongest antibacterial and anti-inflammatory properties among sebaceous fatty acids and strongly enhances the innate antibacterial defence of the skin.

    “Similarly to sapienic acid, oleic acid (18:1Δ9), a major ω9 monounsaturated fatty acid of sebum triglycerides, exerts the strongest antibacterial and anti-inflammatory properties among sebaceous fatty acids and strongly enhances the innate antibacterial defence of the skin.18,19”
    Quote in the paperSubstantial claim1 of 2 sources checked
    • cites [18] Nakatsuji T, Kao MC, Zhang L, Zouboulis CC, Gallo RL, Huang C-M Sebum free fatty acids enhance the innate immune defense of human sebocytes by upregulating β-defensin-2 expression. J Invest Dermatol. 2010; 130: 985– 94. doi: 10.1038/jid.2009.384. PMID:20032992. 20032992 PMC3057125 source

      Split into 2 atoms — 0 confirmed, 2 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.

      Experimental — accuracy not yet measured
    • cites [19] Chen CH, Wang Y, Nakatsuji T, Liu YT, Zouboulis CC, Gallo R, et al. An innate bactericidal oleic acid effective against skin infection of methicillin-resistant staphylococcus aureus: A therapy concordant with evolutionary medicine. J Microbiol Biotechnol. 2011; 21: 391– 9. PMID:21532323. 21532323 source

  • May combine two claims.

    Premisecitation

    Palmitic acid provides direct antibacterial activities against Propionibacterium acnes and enhances the skin innate antibacterial defence by inducing the expression of human β-defensin-2 (hBD2) in human sebocytes and mouse skin.

    “however, it provides direct antibacterial activities against Propionibacterium acnes (P. acnes) and enhances the skin innate antibacterial defence by inducing the expression of human β-defensin-2 (hBD2) in human sebocytes and mouse skin.18”
    Quote in the paperSubstantial claim1 of 1 sources checked
    • cites [18] Nakatsuji T, Kao MC, Zhang L, Zouboulis CC, Gallo RL, Huang C-M Sebum free fatty acids enhance the innate immune defense of human sebocytes by upregulating β-defensin-2 expression. J Invest Dermatol. 2010; 130: 985– 94. doi: 10.1038/jid.2009.384. PMID:20032992. 20032992 PMC3057125 source

      The Discussion reports that palmitic acid increased hBD-2 expression in human sebocytes, supporting the indirect-defense part of the claim. But it says palmitic acid did not have potent bactericidal activity against P. acnes. The mouse-skin Results tested oleic acid, not palmitic acid, and measured mouse β-defensin-4 rather than human hBD-2; page numbers are unavailable in our copy. (LLM, conf=0.91)

      Experimental — accuracy not yet measured

  • Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

    Premisecitation

    Peroxidated squalene along with unsaturated free fatty acids has been reported to be comedogenic and responsible for pathological skin conditions.

    “On the other hand, peroxidated squalene along with unsaturated free fatty acids (FFA), has been reported to be comedogenic and therefore responsible for pathological skin conditions.8,9”
    Quote in the paperNot a substantial claim2 of 2 sources checked
    • cites [8] Chiba K, Yoshizawa K, Makino I, Kawakami K, Onoue M Comedogenicity of squalene monohydroperoxide in the skin after topical application. J Toxicol Sci. 2000; 25: 77– 83. doi: 10.2131/jts.25.77. PMID:10845185. 10845185 source

      The Results (p. 4) report comedone formation after topical application of squalene monohydroperoxide to rabbit ears. The Discussion (p. 6) suggests a role in acne, but does not establish that it is responsible for pathological skin conditions in humans. The Introduction (p. 1) mentions fatty acids as compounds used in comedogenicity studies, without establishing the claim for unsaturated free fatty acids. (LLM, conf=0.87)

      Experimental — accuracy not yet measured
    • cites [9] Leyden JJ New understandings of the pathogenesis of acne. J Am Acad Dermatol. 1995; 32: S15−25. doi: 10.1016/0190-9622(95)90416-6. PMID:7738222. 7738222 source

      In “The follicular canal in acne” (page not provided), the paper reports that squalene and free fatty acids are comedogenic in a rabbit-ear model and discusses squalene peroxides as a possible contributor to comedogenesis. It does not specifically identify unsaturated free fatty acids as the comedogenic group, and its tentative account of acne does not establish that these lipids are responsible for pathological skin conditions generally. (LLM, conf=0.85)

      Experimental — accuracy not yet measured

  • May combine two claims.

    Premisecitation

    Decreased level of vitamin E in acne subjects leads to inflammation and underlines a general importance of lipid peroxidation in the development of acne.

    “Furthermore, studies also detected decreased level of vitamin E in acne subjects, which also leads to inflammation and underlines a general importance of lipid peroxidation in the development of acne.3”
    Quote in the paperNot a substantial claim1 of 1 sources checked
    • cites [3] Picardo M, Ottaviani M, Camera E, Mastrofrancesco A Sebaceous gland lipids. Dermato-endocrinology. 2009; 1: 68– 71. doi: 10.4161/derm.1.2.8472. PMID:20224686. 20224686 PMC2835893 source

      The passage labeled Abstract reports lower vitamin E levels and more squalene peroxide in acne subjects, and says these findings support a role for lipid peroxidation in acne development. Another passage labeled Abstract reports that squalene peroxide induces inflammatory mediators and that vitamin E helps limit its harmful effects. It does not establish that decreased vitamin E itself leads to inflammation. (LLM, conf=0.86)

      Experimental — accuracy not yet measured

  • May combine two claims.

    Premisecitation

    Malassezia lipases and phosphatases hydrolyse sebaceous lipids, resulting in decreased triglycerides and a corresponding increase in free fatty acids, which may cause irritation.

    “In relation to seborrheic dermatitis, studies suggest that the lipases and phosphatases produced by Malassezia hydrolyse sebaceous lipids, resulting in decreased triglycerides and a corresponding increase in FFA, which may cause irritation.30”
    Quote in the paperSubstantial claim1 of 1 sources checked
    • cites [30] DeAngelis YM, Saunders CW, Johnstone KR, Reeder NL, Coleman CG, Kaczvinsky JR Jr., Gale C, Walter R, Mekel M, Lacey MP, et al. Isolation and expression of a Malassezia globosa lipase gene, LIP1. J Invest Dermatol. 2007; 127: 2138– 46. doi: 10.1038/sj.jid.5700844. PMID:17460728. 17460728 source

      The Discussion (page not specified in our copy) says Malassezia can lower triglyceride levels and increase free fatty acids, and presents lipase-mediated hydrolysis and irritation as a proposed model for dandruff and seborrheic dermatitis. The paper does not attribute this hydrolysis to phosphatases, so that part of the claim is unsupported. (LLM, conf=0.88)

      Experimental — accuracy not yet measured

  • May combine two claims.

    Premisecitation

    Dietary palmitic acid activates both the NLRP3 inflammasome and mTORC1.

    “and activates both the NLRP3 inflammasome and mTORC116,17”
    Quote in the paperNot a substantial claim2 of 2 sources checked
    • cites [16] Yasuda M, Tanaka Y, Kume S, Morita Y, Chin-Kanasaki M, Araki H, Isshiki K, Araki S, Koya D, Haneda M, et al. Fatty acids are novel nutrient factors to regulate mTORC1 lysosomal localization and apoptosis in podocytes. Biochimica et biophysica acta. 2014; 1842: 1097– 108. doi: 10.1016/j.bbadis.2014.04.001. PMID:24726883. 24726883 source

      Section 3.2 reports that palmitate activated mTORC1 signaling in cultured podocytes, and Section 3.4 links this to mTOR translocation onto lysosomal membranes (page numbers unavailable). The cited paper does not establish that dietary palmitic acid activates mTORC1, and the passages do not address NLRP3 inflammasome activation. (LLM, conf=0.88)

      Experimental — accuracy not yet measured
    • cites [17] Legrand-Poels S, Esser N, L'Homme L, Scheen A, Paquot N, Piette J Free fatty acids as modulators of the NLRP3 inflammasome in obesity/type 2 diabetes. Biochemical pharmacology. 2014; 92: 131– 41. doi: 10.1016/j.bcp.2014.08.013. PMID:25175736. 25175736 source

      Section 4 reports that palmitate activated the NLRP3 inflammasome in LPS-primed macrophages, supporting that part of the claim in a specific cell-culture setting. The passages found do not report that palmitate activates mTORC1 or establish the claim for dietary palmitic acid. (LLM, conf=0.87)

      Experimental — accuracy not yet measured

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    Elongation and further desaturation of sapienic acid yields sebaleic acid (18:2Δ5,8).

    “The elongation and further desaturation of sapienic acid yields another unique sebaceous gland fatty acid, sebaleic acid (18:2Δ5, 8).3”
    Quote in the paperNot a substantial claim1 of 1 sources checked
    • cites [3] Picardo M, Ottaviani M, Camera E, Mastrofrancesco A Sebaceous gland lipids. Dermato-endocrinology. 2009; 1: 68– 71. doi: 10.4161/derm.1.2.8472. PMID:20224686. 20224686 PMC2835893 source

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    Healthy human skin is populated with a characteristic microbiome.

    “The healthy human skin is populated with a characteristic microbiome.54”
    Quote in the paperNot a substantial claim1 of 1 sources checked
    • cites [54] Grice EA, Segre JA The skin microbiome. Nat Rev Microbiol. 2011; 9: 244– 53. doi: 10.1038/nrmicro253710.1038/nrmicro2619. PMID:21407241. 21407241 PMC3535073 source

  • May combine two claims.

    Interpretationcitation

    Individual sensitivity to the irritating free fatty acids determines the consequent inflammatory response and may define susceptibility for seborrheic dermatitis.

    “Therefore, individual sensitivity to the irritating FFA determines the consequent inflammatory response and may define susceptibility for seborrheic dermatitis.31”
    Quote in the paperSubstantial claim1 of 1 sources checked
    • cites [31] Thayikkannu AB, Kindo AJ, Veeraraghavan M Malassezia-Can it be Ignored? Indian journal of dermatology. 2015; 60: 332– 9. doi: 10.4103/0019-5154.160475. PMID:26288399. 26288399 PMC4533528 source

      The Clinical scenario section says Malassezia breaks down sebum into irritating fatty acids that initiate inflammation. It also discusses host susceptibility to seborrheic dermatitis, but does not say that individual sensitivity to those fatty acids determines the inflammatory response or susceptibility. No page number is available in our copy. (LLM, conf=0.82)

      Experimental — accuracy not yet measured

  • May combine two claims.

    Premisecitation

    Sebaceous lipids make an important contribution in maintaining the integrity of the skin barrier along with lipids of epidermal origin, thus contributing to the body's first line of defence.

    “Moreover, sebaceous lipids make an important contribution in maintaining the integrity of the skin barrier along with lipids of epidermal origin2,52 thus contributing to the body's first line of defence.53”
    Quote in the paperNot a substantial claim1 of 3 sources checked
    • cites [2] Zouboulis CC, Baron JM, Bohm M, Kippenberger S, Kurzen H, Reichrath J, Thielitz A Frontiers in sebaceous gland biology and pathology. Exp Dermatol. 2008; 17: 542– 51. doi: 10.1111/j.1600-0625.2008.00725.x. PMID:18474083. 18474083 source
    • cites [52] Zouboulis CC Acne and sebaceous gland function. Clinics in dermatology. 2004; 22: 360– 6. doi: 10.1016/j.clindermatol.2004.03.004. PMID:15556719. 15556719 source
    • cites [53] Zouboulis CC, Picardo M, Ju Q, Kurokawa I, Torocsik D, Biro T, Schneider MR Beyond acne: Current aspects of sebaceous gland biology and function. Reviews in endocrine & metabolic disorders. 2016;17(3):319–334. doi: 10.1007/s11154-016-9389-5. PMID:27726049. 27726049 source

  • May combine two claims.

    Premisecitation

    Both testosterone and 5α-DHT increase sebaceous proliferation.

    “Both testosterone and 5α-DHT increase sebaceous proliferation, however, they do not affect lipid synthesis.68,69”
    Quote in the paperNot a substantial claim1 of 2 sources checked
    • cites [68] Fritsch M, Orfanos CE, Zouboulis CC Sebocytes are the key regulators of androgen homeostasis in human skin. J Invest Dermatol. 2001; 116: 793– 800. doi: 10.1046/j.1523-1747.2001.01312.x. PMID:11348472. 11348472 source

      The introductory passage (p. 793) reports that testosterone stimulates sebum secretion, not sebaceous proliferation. The testosterone-metabolism results and Discussion (pp. 793–800) address conversion to 5α-DHT but do not report whether either androgen increases sebaceous proliferation. Searches for proliferation and cell growth found no passage establishing the claim. (LLM, conf=0.76)

      Experimental — accuracy not yet measured
    • cites [69] Akamatsu H, Zouboulis CC, Orfanos CE Control of human sebocyte proliferation in vitro by testosterone and 5-alpha-dihydrotestosterone is dependent on the localization of the sebaceous glands. J Invest Dermatol 1992; 99: 509– 11. doi: 10.1111/1523-1747.ep12616181. PMID:1402009. 1402009 source

  • May combine two claims.

    Premisecitation

    These antimicrobials act as part of the innate immune system of the skin and are generated through the action of ceramidases from the stratum corneum.

    “These antimicrobials act as part of the innate immune system of the skin, and are generated through the action of ceramidases from the stratum corneum.63”
    Quote in the paperNot a substantial claim1 of 1 sources checked
    • cites [63] Fischer CL, Blanchette DR, Brogden KA, Dawson DV, Drake DR, Hill JR, Wertz PW The roles of cutaneous lipids in host defense. Biochimica et biophysica acta. 2014; 1841: 319– 22. doi: 10.1016/j.bbalip.2013.08.012. PMID:23994607. 23994607 PMC3943473 source

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    One of the major factors in human sebaceous lipogenesis is the hormonal changes taking place at puberty.

    “One of the major factors in humans are the hormonal changes taking place at puberty.67”
    Quote in the paperNot a substantial claim1 of 1 sources checked
    • cites [67] Zouboulis CC, Chen WC, Thornton MJ, Qin K, Rosenfield R Sexual hormones in human skin. Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et metabolisme. 2007; 39: 85– 95. doi: 10.1055/s-2007-961807. PMID:17326004. 17326004 source

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    LXR receptors have a well-defined role in cellular cholesterol homeostasis and lipid metabolism.

    “The Liver X Receptor (LXR) receptors which have a well-defined role in cellular cholesterol homeostasis and lipid metabolism75,76”
    Quote in the paperNot a substantial claim1 of 2 sources checked
    • cites [75] Torocsik D, Szanto A, Nagy L Oxysterol signaling links cholesterol metabolism and inflammation via the liver X receptor in macrophages. Molecular aspects of medicine. 2009; 30: 134– 52. doi: 10.1016/j.mam.2009.02.002. PMID:19248804. 19248804 source
    • cites [76] Zouboulis CC Sebaceous gland receptors. Dermato-endocrinology. 2009; 1: 77– 80. doi: 10.4161/derm.1.2.7804. PMID:20224688. 20224688 PMC2835895 source

      The Sebocyte Receptors section (page not available) reports that LXR ligands increase lipogenesis in SZ95 sebocytes and induce lipid-synthesis targets, supporting a role in lipid metabolism. It does not describe a role in cellular cholesterol homeostasis, and its discussion is limited to sebocytes rather than cells generally. (LLM, conf=0.85)

      Experimental — accuracy not yet measured

  • May combine two claims.

    Premisecitation

    Corticotropin-releasing hormone is expressed in human sebocytes and augments the synthesis of sebaceous lipids in vitro.

    “Corticotropin-releasing hormone is expressed in human sebocytes and augments the synthesis of sebaceous lipids in vitro.85,79”
    Quote in the paperNot a substantial claim2 of 2 sources checked
    • cites [85] Zouboulis CC, Seltmann H, Hiroi N, Chen W, Young M, Oeff M, Scherbaum WA, Orfanos CE, McCann SM, Bornstein SR Corticotropin-releasing hormone: an autocrine hormone that promotes lipogenesis in human sebocytes. Proceedings of the National Academy of Sciences of the United States of America. 2002; 99: 7148– 53. doi: 10.1073/pnas.102180999. PMID:12011471. 12011471 PMC124543 source
    • cites [79] Tsukada M, Schroder M, Roos TC, Chandraratna RA, Reichert U, Merk HF, Orfanos CE, Zouboulis CC 13-cis retinoic acid exerts its specific activity on human sebocytes through selective intracellular isomerization to all-trans retinoic acid and binding to retinoid acid receptors. J Invest Dermatol. 2000; 115: 321– 7. doi: 10.1046/j.1523-1747.2000.00066.x. PMID:10951254. 10951254 source

      The Materials and Methods and Discussion passages address retinoid treatment of human sebocytes, not corticotropin-releasing hormone. Searches for “corticotropin-releasing hormone” and “CRH” found no passage in our copy addressing its expression in sebocytes or its effect on sebaceous lipid synthesis. Page numbers were not available in the indexed copy. (LLM, conf=0.76)

      Experimental — accuracy not yet measured

  • May combine two claims.

    Premisecitation

    Human sebocytes express melanocortin 5 receptor (MC5R), which is involved in sebocyte differentiation and lipogenesis.

    “Human sebocytes also express melanocortin 5 receptor (MC5R), which is involved in sebocyte differentiation and lipogenesis.87,88”
    Quote in the paperNot a substantial claim1 of 2 sources checked
    • cites [87] Thiboutot D, Sivarajah A, Gilliland K, Cong Z, Clawson G The melanocortin 5 receptor is expressed in human sebaceous glands and rat preputial cells. J Invest Dermatol. 2000; 115: 614– 9. doi: 10.1046/j.1523-1747.2000.00094.x. PMID:10998132. 10998132 source

      The Discussion reports MC5R expression in human sebaceous glands and cultured human sebocytes. It discusses differentiation as a subject for further study, but explicitly says that MC5R’s role in regulating human sebum production has not been established. It therefore does not establish that MC5R is involved in human sebocyte differentiation or lipogenesis. (LLM, conf=0.91)

      Experimental — accuracy not yet measured
    • cites [88] Zhang L, Li WH, Anthonavage M, Eisinger M Melanocortin-5 receptor: a marker of human sebocyte differentiation. Peptides. 2006; 27: 413– 20. doi: 10.1016/j.peptides.2005.05.030. PMID:16309786. 16309786 source

  • May combine two claims.

    Premisecitation

    Leptin affects lipogenesis by increasing triglyceride levels, increasing the ratio of monounsaturated or polyunsaturated fatty acids to saturated fatty acids, and decreasing the levels of vitamin E.

    “also affects lipogenesis by increasing triglyceride levels, thus increasing the ratio of monounsaturated fatty acids or polyunsaturated fatty acids to saturated fatty acids and by decreasing the levels of vitamin E”
    Quote in the paperNot a substantial claim1 of 3 sources checked
    • cites [24] Ottaviani M, Camera E, Picardo M Lipid mediators in acne. Mediators of inflammation. 2010; 2010. doi: 10.1155/2010/858176. PMID: 20871834 20871834 PMC2943135 source

      Section 3.3 reports lower vitamin E in acne sebum, and section 3.2 reports altered saturated-to-unsaturated fatty-acid ratios in acne. Neither passage attributes these changes to leptin, and searches for leptin and the claimed triglyceride changes found no passage addressing that causal claim. (LLM, conf=0.76)

      Experimental — accuracy not yet measured
    • cites [25] Zouboulis CC, Jourdan E, Picardo M Acne is an inflammatory disease and alterations of sebum composition initiate acne lesions. J Eur Acad Dermatol Venereol. 2014; 28: 527– 32. doi: 10.1111/jdv.12298. PMID:24134468. 24134468 source
    • cites [44] Torocsik D, Kovacs D, Camera E, Lovaszi M, Cseri K, Nagy GG, Molinaro R, Ruhl R, Tax G, Szabo K, et al. Leptin promotes a proinflammatory lipid profile and induces inflammatory pathways in human SZ95 sebocytes. Br J Dermatol. 2014; 171: 1326– 35. doi: 10.1111/bjd.13229. PMID:24975960. 24975960 source

  • May combine two claims.

    Findingown data

    In atopic dermatitis, the proportion of sebaceous lipids in the casual lipids is decreased and epidermal lipids (e.g. cholesterol) are increased, while the total casual lipid amount is barely changed.

    “However, and despite the fact that the proportion of sebaceous lipids in the casual lipids is decreased and epidermal lipids (e.g. cholesterol) are increased, the total casual lipid amount is barely changed (own unpublished data).”
    Quote in the paperNot a substantial claim
    • Rests on an assumption: Atopic dermatitis patients have severely reduced sebum production.

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    Sapienic acid is a unique sebaceous monounsaturated fatty acid with a single double bond at the sixth position.

    “Sapienic acid is a unique sebaceous monounsaturated fatty acid with a single double bond at the sixth position.12,13”
    Quote in the paperNot a substantial claim0 of 2 sources checked
    • cites [12] Nicolaides N Skin lipids: their biochemical uniqueness. Science 1974; 186: 19– 26. doi: 10.1126/science.186.4158.19. PMID:4607408. 4607408 source
    • cites [13] Stewart ME, Owen Grahek M, Cambier LS, Wertz PW, Downing DT Dilutional effect of increased sebaceous gland activity on the proportion of linoleic acid in sebaceous wax esters and in epidermal acylceramides.] Invest Dermatol 1986; 87: 733– 6. 2946783 source

  • May combine two claims.

    Premisecitation

    Sapienic acid exerts strong antibacterial and antifungal activities.

    “Sapienic acid exerts strong antibacterial and antifungal activities.14”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [14] Wille JJ, Kydonieus A Palmitoleic acid isomer (C16:1Δ6) in human skin sebum is effective against gram-positive bacteria. Skin Pharmacol Physiol. 2003; 16: 176– 87. doi: 10.1159/000069757. 12677098 source

  • Probably not a substantial claim: may not pass S4 (based).

    Interpretationnone given

    Variations in the composition and amount of sebum in different skin diseases are suggested to not be simply disease markers but may also play a significant role in disease pathogenesis.

    “Variations in the composition and amount of sebum in different skin diseases have been detected, which are suggested to not be simply disease markers but may also play a significant role in disease pathogenesis.”
    Quote in the paperNot a substantial claim

  • May combine two claims.

    Premisecitation

    Sebaceous glands secrete acids that form the acid mantle, a slightly acidic (between pH 4.5 and pH 6.0) film on the surface of the skin that provides a barrier against pathogens such as bacteria and viruses.

    “Sebaceous glands secrete acids that form the acid mantle, a fine, slightly acidic (between pH 4.5 and pH 6.0) film on the surface of the skin that provides a barrier against pathogens, such as bacteria and viruses that might penetrate the skin and are primarily of alkaline nature.51”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [51] Schmid-Wendtner MH, Korting HC The pH of the skin surface and its impact on the barrier function. Skin pharmacology and physiology. 2006; 19: 296– 302. doi: 10.1159/000094670. PMID:16864974. 16864974 source

  • May combine two claims.

    Interpretationcitation

    A link between an altered sebaceous gland function and skin barrier dysfunction seems to contribute to the development of atopic dermatitis, although the exact mechanisms have not been elucidated.

    “Therefore, a link between an altered sebaceous gland function and skin barrier dysfunction seem to contribute to the development of the disease, although the exact mechanisms have not been elucidated.40,41”
    Quote in the paperSubstantial claim0 of 2 sources checked
    • cites [40] Firooz A, Gorouhi F, Davari P, Atarod M, Hekmat S, Rashighi-Firoozabadi M, Solhpour A Comparison of hydration, sebum and pH values in clinically normal skin of patients with atopic dermatitis and healthy controls. Clinical and experimental dermatology. 2007; 32: 321– 2. doi: 10.1111/j.1365-2230.2007.02364.x. PMID:17335552. 17335552 source
    • cites [41] Wirth H, Gloor M, Stoika D Sebaceous glands in uninvolved skin of patients suffering from atopic dermatitis. Arch Dermatol Res. 1981; 270: 167– 9. doi: 10.1007/BF00408228. PMID:7247453. 7247453 source
    • Rests on an assumption: Atopic dermatitis patients have severely reduced sebum production.

  • May combine two claims.

    Premisecitation

    Affected rosacea individuals exhibit elevated levels of myristic acid (C14:0) and reduced levels of saturated long chain fatty acids.

    “Affected individuals exhibit elevated levels of myristic acid (C14:0) and reduced levels of saturated long chain fatty acids.33”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [33] Ni Raghallaigh S, Bender K, Lacey N, Brennan L, Powell FC The fatty acid profile of the skin surface lipid layer in papulopustular rosacea. Br J Dermatol. 2012; 166: 279– 87. doi: 10.1111/j.1365-2133.2011.10662.x. PMID:21967555. 21967555 source

  • May combine two claims.

    Premisecitation

    Bacterial lipase activity leads to an increased presence of free fatty acids on the surface of the skin and to an altered sebum composition.

    “This bacterial lipase activity not only leads to an increased presence of FFA on the surface of the skin, but also to an altered sebum composition.58”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [58] Drake DR, Brogden KA, Dawson DV, Wertz PW Thematic review series: skin lipids. Antimicrobial lipids at the skin surface. J Lipid Res. 2008; 49: 4– 11. doi: 10.1194/jlr.R700016-JLR200. PMID:17906220. 17906220 source

  • May combine two claims.

    Premisecitation

    The IGF-1 receptor is present in sebocytes and activates the PI3K/Akt/FoxO1 pathway.

    “The presence of the IGF-1 receptor in sebocytes has been described and was shown to activate the PI3K/ Akt/FoxO1 pathway”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [84] Mirdamadi Y, Thielitz A, Wiede A, Goihl A, Papakonstantinou E, Hartig R, Zouboulis CC, Reinhold D, Simeoni L, Bommhardt U, et al. Insulin and insulin-like growth factor-1 can modulate the phosphoinositide-3-kinase/Akt/FoxO1 pathway in SZ95 sebocytes in vitro. Molecular and cellular endocrinology. 2015; 415: 32– 44. doi: 10.1016/j.mce.2015.08.001. PMID:26257240. 26257240 source

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    PPAR-α seems to be related to β-oxidation of fatty acids and lipid catabolism.

    “Furthermore, PPAR-α seems to be related to β-oxidation of fatty acids and lipid catabolism.73”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [73] Trivedi NR, Cong Z, Nelson AM, Albert AJ, Rosamilia LL, Sivarajah S, Gilliland KL, Liu W, Mauger DT, Gabbay RA, et al. Peroxisome proliferator-activated receptors increase human sebum production. J Invest Dermatol. 2006; 126: 2002– 9. doi: 10.1038/sj.jid.5700336. PMID:16675962. 16675962 source

  • May combine two claims.

    Interpretationcitation

    Sebum lipids not only can regulate macrophage function, but also integrate into disease-specific settings, such as acne.

    “These results shed light on how sebum composition plays a key role in regulating immune responses against bacteria, such as P. acnes, proving that sebum lipids not only can regulate macrophage function, but also integrate into disease-specific settings, such as acne.25”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [25] Zouboulis CC, Jourdan E, Picardo M Acne is an inflammatory disease and alterations of sebum composition initiate acne lesions. J Eur Acad Dermatol Venereol. 2014; 28: 527– 32. doi: 10.1111/jdv.12298. PMID:24134468. 24134468 source

  • May combine two claims.

    Premisecitation

    Sebaceous glands not only respond to androgens, but are also capable of producing them.

    “Sebaceous glands not only respond to androgens, but are also capable of producing them.”
    Quote in the paperNot a substantial claim

  • May combine two claims.

    Interpretationreasoning

    These changes lead to hyperkeratinisation and chronic inflammation, which further increases the pathological microbial colonization of the skin, thus sustaining acne formation.

    “These changes lead to hyperkeratinisation and chronic inflammation, which further increases the pathological microbial colonization of the skin, thus sustaining acne formation.”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Premisecitation

    The ligands all-trans retinoic acid (atRA) and 9-cis-retinoic acid (9cRA) inhibit sebocyte differentiation and lipid synthesis.

    “and their ligands all-trans retinoic acid (atRA) and 9-cis-retinoic acid (9cRA) inhibit sebocyte differentiation and lipid synthesis.80”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [80] Zouboulis CC, Korge B, Akamatsu H, Xia LQ, Schiller S, Gollnick H, Orfanos CE Effects of 13-cis-retinoic acid, all-trans-retinoic acid, and acitretin on the proliferation, lipid synthesis and keratin expression of cultured human sebocytes in vitro. J Invest Dermatol. 1991; 96: 792– 7. doi: 10.1111/1523-1747.ep12471782. PMID:1708801. 1708801 source

  • May combine two claims.

    Premisecitation

    RAR-α and -γ and RXR-α, -β, -γ are expressed in human sebocytes.

    “Both retinoic acid receptors (RAR-α and -γ) and retinoid X receptors (RXR-α, -β, -γ) are expressed in human sebocytes”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [80] Zouboulis CC, Korge B, Akamatsu H, Xia LQ, Schiller S, Gollnick H, Orfanos CE Effects of 13-cis-retinoic acid, all-trans-retinoic acid, and acitretin on the proliferation, lipid synthesis and keratin expression of cultured human sebocytes in vitro. J Invest Dermatol. 1991; 96: 792– 7. doi: 10.1111/1523-1747.ep12471782. PMID:1708801. 1708801 source

  • May combine two claims.

    Premisecitation

    PPAR-α, -δ, -γ1 and -γ2 are all expressed in sebocytes.

    “PPARs with all three isoforms namely PPAR-α, -δ, -γ1 and -γ2 which are all expressed in sebocytes47”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [47] Alestas T, Ganceviciene R, Fimmel S, Muller-Decker K, Zouboulis CC Enzymes involved in the biosynthesis of leukotriene B4 and prostaglandin E2 are active in sebaceous glands. Journal of molecular medicine (Berlin, Germany). 2006; 84: 75– 87. doi: 10.1007/s00109-005-0715-8. PMID:16388388. 16388388 source

  • May combine two claims.

    Premisecitation

    Arachidonoyl ethanolamide/anandamide and 2-arachidonoyl glycerol are present in sebocytes and can induce lipid production and apoptosis.

    “more interestingly arachidonoyl ethanolamide/anandamide, 2-arachidonoyl glycerol are also present in sebocytes and can induce lipid production and apoptosis.42”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [42] Dobrosi N, Toth BI, Nagy G, Dozsa A, Geczy T, Nagy L, Zouboulis CC, Paus R, Kovacs L, Biro T Endocannabinoids enhance lipid synthesis and apoptosis of human sebocytes via cannabinoid receptor-2-mediated signaling. FASEB journal: official publication of the Federation of American Societies for Experimental Biology. 2008; 22: 3685– 95. doi: 10.1096/fj.07-104877. PMID:18596221. 18596221 source

  • May combine two claims.

    Interpretationreasoning

    Sebaceous gland lipids have been shown to exhibit pro- and anti-inflammatory properties, attributed with antimicrobial qualities, and most recently they have been demonstrated to exert a modulating role on immune cells.

    “Sebaceous gland lipids have been shown to exhibit pro-and anti-inflammatory properties, attributed with antimicrobial qualities and most recently they have been demonstrated to exert a modulating role on immune cells (Fig. 1).”
    Quote in the paperSubstantial claim
38 of 38

  • The authors state this as an assumption.

    The altered sebaceous fatty acid profile is an important contributor to skin barrier dysfunction leading to rosacea.

    “These lipids have a role in maintaining the skin barrier integrity, therefore it is reasonable to assume that the altered sebaceous fatty acid profile is an important contributor to skin barrier dysfunction leading to rosacea.33”

  • The paper relies on this without support.

    Atopic dermatitis patients have severely reduced sebum production.

    “Although AD is mainly characterized by the dysfunctional synthesis of ceramides in keratinocytes39, AD patients seem to exert a severely reduced sebum production, which should contribute to diminished skin hydration.”
2 of 2

Cites

Flagged first, then by citations

Research works printed but not linked: 4

  1. 10.1038/jid.1953.9810.1038/jid.1953.67 · DOI
  2. 10.1038/jid.1953.6710.1038/jid.1953.98 · DOI
  3. 10.1038/nrmicro253710.1038/nrmicro2619 · DOI
  4. 10.1016/j.jid.2017.07.64310.1016/j.jid.2016.12.025 · DOI

Cited by

Sorted by citations

Related

Authors
Lovászi, M., Szegedi, A., Zouboulis, C. C., & Törőcsik, D.
Affiliations
  • University of Debrecen (HU)
  • Medizinische Hochschule Brandenburg Theodor Fontane (DE)
Corresponding author
Törőcsik, Dániel
ORCID
Venue
Dermato-Endocrinology
Publisher
Informa UK Limited
Published
2017-01-01
Volume
9
Issue
1
Pages
e1375636-e1375636
ISSN
  • 1938-1972 (ISSN-L)
  • 1938-1980
DOI
10.1080/19381980.2017.1375636
PMC
PMC5821166
OpenAlex
W2762894008
Semantic Scholar
bdddc896532e6450af27244d27cd660c49a516f1
Cited by
151
References
93
Citations by year
2026: 14 · 2025: 14 · 2024: 28 · 2023: 28 · 2022: 18 · 2021: 26 · 2020: 11 · 2019: 6 · 2018: 4
FWCI
5.73
Type
journal article
Language
en
Open access
Licence
Locations
  • Dermato-Endocrinology (publishedVersion, cc-by-nc)
  • PubMed (publishedVersion)
  • University of Debrecen Electronic Archive (University of Debrecen) (submittedVersion, cc-by-nc)
  • Europe PMC (PubMed Central) (submittedVersion, cc-by-nc)
  • PubMed Central (submittedVersion, cc-by-nc)
  • University of Debrecen Electronic Archive (University of Debrecen) (submittedVersion)
  • University of Debrecen Electronic Archive (University of Debrecen) (submittedVersion, other-oa)
Funders
  • Hungarian National Research Found (OTKA NN117020 NKFIH K108421)
  • New National Excellence Program of the Ministry of Human Capacities (GINOP-2.3.2-15-2016-00050, GINOP-2.3.2-15-2016-00005)
Topics
  • Health Sciences › Medicine › Dermatology › Dermatology and Skin Diseases
  • Health Sciences › Medicine › Dermatology › Acne and Rosacea Treatments and Effects
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Lipid metabolism and biosynthesis
Keywords
sebaceous glands, sebum lipids, macrophages, keratinocytes, skin disease pathogenesis

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Claims read by deepseek-v4.1-flash under definition version 3 (extract-v3) on 2026-10-22.

Classified by jev-1.13-20260917 (gold-guideline-v0.2) on 2026-10-22.

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Statistics and arithmetic are recomputed, not judged.

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