Elevated survivin levels in patients with acne vulgaris

Saraç, Gülhan Aksoy; Kader, Saadet; Akdağ, Turan

doi:10.1111/jocd.14742

Cited by 5 publications

(2 citation statements)

References 25 publications

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“…In recent research by Kader and Akda [32] , acne sufferers exhibited serum survivin levels that were significantly greater (153.4 pg/ml) than the control group (104.2 pg/ml). Also, there was a substantial association between the SCAR-S score and survivin levels as well as a positive relationship between survivin and the severity of the acne.…”

Section: Discussionmentioning

confidence: 88%

Survivin Gene Polymorphism in Association with Plasma Survivin Level as Potential Risk Factors for Acne Severity and Post-Acne Scaring

State¹,

El-Sohafy²,

Salam³

et al. 2023

The Egyptian Journal of Hospital Medicine

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Background: Acne vulgaris is the most common cutaneous ailment in the world, affecting up to 80% of teenagers and up to 50% of adults. It is a chronic inflammatory disease of the pilosebaceous unit. The development of acne lesions is heavily influenced by keratinocyte proliferative and inflammatory states, which have been observed to elevate survivin levels.Objective: This study was conducted to assess survivin gene polymorphism and its plasma level in patients with active acne vulgaris and patients with post acne scars with varying severity. Patients and methods:The study included 60 acne patients divided into two groups: 30 patients with active acne lesions and 30 patients with post acne scars; in addition to 30 healthy volunteers who were served as control group selected from Outpatient Clinic,

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Section: Discussionmentioning

confidence: 88%

Survivin Gene Polymorphism in Association with Plasma Survivin Level as Potential Risk Factors for Acne Severity and Post-Acne Scaring

State¹,

El-Sohafy²,

Salam³

et al. 2023

The Egyptian Journal of Hospital Medicine

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“…Importantly, p53 upregulates the expression of the proapoptotic proteins TRAIL (TNFSF10) [217], FoxO1 (FOXO1A) [176,177] and FoxO3 (FOXO3A) [176], respectively. In contrast, survivin (BIRC5), a member of the inhibitors of the apoptosis gene family, which is overexpressed in the serum of acne patients [218,219], is suppressed by p53 [220]. Thus, the isotretinoin-mediated upregulation of nuclear p53 in SGs [179] most likely represents the desired sebum-suppressive effect in promoting sebocyte apoptosis.…”

Section: Sebum Suppression Sebocyte Autophagy and Apoptosismentioning

confidence: 99%

Acne Transcriptomics: Fundamentals of Acne Pathogenesis and Isotretinoin Treatment

Melnik

2023

Cells

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This review on acne transcriptomics allows for deeper insights into the pathogenesis of acne and isotretinoin’s mode of action. Puberty-induced insulin-like growth factor 1 (IGF-1), insulin and androgen signaling activate the kinase AKT and mechanistic target of rapamycin complex 1 (mTORC1). A Western diet (hyperglycemic carbohydrates and milk/dairy products) also co-stimulates AKT/mTORC1 signaling. The AKT-mediated phosphorylation of nuclear FoxO1 and FoxO3 results in their extrusion into the cytoplasm, a critical switch which enhances the transactivation of lipogenic and proinflammatory transcription factors, including androgen receptor (AR), sterol regulatory element-binding transcription factor 1 (SREBF1), peroxisome proliferator-activated receptor γ (PPARγ) and signal transducer and activator of transcription 3 (STAT3), but reduces the FoxO1-dependent expression of GATA binding protein 6 (GATA6), the key transcription factor for infundibular keratinocyte homeostasis. The AKT-mediated phosphorylation of the p53-binding protein MDM2 promotes the degradation of p53. In contrast, isotretinoin enhances the expression of p53, FoxO1 and FoxO3 in the sebaceous glands of acne patients. The overexpression of these proapoptotic transcription factors explains isotretinoin’s desirable sebum-suppressive effect via the induction of sebocyte apoptosis and the depletion of BLIMP1(+) sebocyte progenitor cells; it also explains its adverse effects, including teratogenicity (neural crest cell apoptosis), a reduced ovarian reserve (granulosa cell apoptosis), the risk of depression (the apoptosis of hypothalamic neurons), VLDL hyperlipidemia, intracranial hypertension and dry skin.

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The Therapeutic Mechanisms of Huayu Quban Capsule in Treating Acne Vulgaris Are Uncovered Through Network Pharmacology and Molecular Docking

Zhang,

Huang,

Zhu

2024

J of Cosmetic Dermatology

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PurposeTo uncover how the Huayu Quban (HYQB) capsule treats acne vulgaris (AV) through the use of network pharmacology and molecular docking technology.MethodsThe traditional Chinese medicine system pharmacology database (TCMSP) was used to identify the components and potential targets of HYQB capsule. Targets related to AV were identified by screening the GeneCards, Disease Gene Network (DisGeNET) and Online Mendelian Inheritance in Man (OMIM) databases. The protein–protein interaction (PPI) network between targets of active ingredients and AV targets was built using the STRING database. Cytoscape3.7.2 software was used to create the visualization network for the ‘herb‐component‐target’ and identify the key targets. Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) were utilized for functional enrichment analysis of the primary targets. Subsequently, molecular docking technology was employed to confirm the interaction between key components and core targets.ResultsThe technique discovered 50 different active substances and 270 associated therapeutic targets in the HYQB capsule as well as predicting 70 targets for treating acne vulgaris. Cytoscape hubba plug‐in identified 19 key target genes, with the top 5 being TNF, IL1B, CCL2, SIRT1, IFNG, and IL10. Analysis of KEGG pathways revealed significant enrichment of immune‐related pathways, including TNF and IL‐17 signaling pathways, among the target genes. The HYQB capsule also involves lipid and atherosclerosis, Th17 cell differentiation, and the AGE‐RAGE signaling pathway in diabetic complication signaling pathways. Molecular docking results showed that quercetin, luteolin, kaempferol, and wogonin, the core components of HYQB, had good binding ability with the first 4 core targets.ConclusionsThe HYQB capsule may have a synergistic effect on inhibiting sebaceous adipogenesis and sebum cell differentiation and play an effect on AV through anti‐inflammatory and antioxidant effects of different signaling pathways.

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Elevated survivin levels in patients with acne vulgaris

Cited by 5 publications

References 25 publications

Survivin Gene Polymorphism in Association with Plasma Survivin Level as Potential Risk Factors for Acne Severity and Post-Acne Scaring

Survivin Gene Polymorphism in Association with Plasma Survivin Level as Potential Risk Factors for Acne Severity and Post-Acne Scaring

Acne Transcriptomics: Fundamentals of Acne Pathogenesis and Isotretinoin Treatment

The Therapeutic Mechanisms of Huayu Quban Capsule in Treating Acne Vulgaris Are Uncovered Through Network Pharmacology and Molecular Docking

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