Autophagy in Skin Diseases

Guo, Yeye; Zhang, Xu; Wu, Tianhao; Hu, Xing; Su, Juan; Chen, Xiang

doi:10.1159/000500470

Cited by 50 publications

(40 citation statements)

References 120 publications

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“…So autophagy dysfunction could potentiate the action of these pathogens as a triggering factor for psoriasis development. 30 A polymorphism in the Atg16L1 gene has been linked to psoriasis development which is essential for the autophagy pathway. 10 This Atg16L1 gene product has a vital role in dealing with bacterial pathogens and antigen presentation, which could be responsible for psoriasis triggering.…”

Section: Discussionmentioning

confidence: 99%

Assessment of the Effect of Metabolic Syndrome on the Autophagy Marker LC3 in Psoriasis Vulgaris Patients: A Cross-Sectional Study

Nada

Muhammad

Ahmed

et al. 2020

CCID

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Purpose Psoriasis vulgaris, one of the most prevalent chronic inflammatory skin diseases, is associated with metabolic syndrome (MetS). Autophagy, an intracellular degradation system is essential for cell survival and differentiation, and its dysfunction may contribute to metabolic diseases. A cross-sectional study was conducted on 38 psoriasis vulgaris patients and 16 healthy control subjects to 1) Assess immunohistochemical (IHC) expression of microtubule-associated protein light chain 3 (LC3); 2) Evaluate the relationship between Psoriasis Area Severity Index (PASI) score, and LC3 expression. Patients and Methods PASI score was evaluated for all psoriasis patients. Lipid profile, blood sugar, and CRP were done for all patients and controls. A punch biopsy was taken from lesional and perilesional skin of psoriasis patients and normal skin of the controls. Tissue sections were prepared. IHC LC3 staining was done and evaluated. Results LC3 was nearly absent, in the epidermis of the lesional skin of psoriasis while it was strong among control (p=0.001). LC3 expression in the lesional skin of psoriasis vulgaris was lower than its expression in perilesional (p=0.001). However, LC3 expression was not significantly changed with PASI or the presence/absence of MetS. Conclusion A potential link between psoriasis vulgaris and autophagy as assessed by LC3 could be present. LC3 was down-regulated in psoriasis lesions than in normal skin. However, its expression did not change with PASI or MetS. An autophagy enhancer might be used as a possible therapeutic target in psoriasis vulgaris patients.

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Section: Discussionmentioning

confidence: 99%

Assessment of the Effect of Metabolic Syndrome on the Autophagy Marker LC3 in Psoriasis Vulgaris Patients: A Cross-Sectional Study

Nada

Muhammad

Ahmed

et al. 2020

CCID

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“…Following dysregulation of the cell cycle, autophagy and apoptosis have important roles in inflammatory processes (72) underlying both OP and Pso. This could represent a further mechanism through which vitamin D deficiency contributes to their pathogeneses (73)(74)(75)(76). In psoriatic skin inflammation, cytokines and chemokines produced by dysregulated T lymphocytes play key roles (77).…”

Section: The Role Of Vitamin Dmentioning

confidence: 99%

IL-33/Vitamin D Crosstalk in Psoriasis-Associated Osteoporosis

et al. 2021

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Patients with psoriasis (Pso) and, in particular, psoriatic arthritis (PsoA) have an increased risk of developing osteoporosis (OP). It has been shown that OP is among the more common pathologies associated with Pso, mainly due to the well-known osteopenizing conditions coexisting in these patients. Pso and OP share common risk factors, such as vitamin D deficiency and chronic inflammation. Interestingly, the interleukin (IL)-33/ST2 axis, together with vitamin D, is closely related to both Pso and OP. Vitamin D and the IL-33/ST2 signaling pathways are closely involved in bone remodeling, as well as in skin barrier pathophysiology. The production of anti-osteoclastogenic cytokines, e.g., IL-4 and IL-10, is promoted by IL-33 and vitamin D, which are stimulators of both regulatory and Th2 cells. IL-33, together with other Th2 cytokines, shifts osteoclast precursor differentiation towards macrophage and dendritic cells and inhibits receptor activator of nuclear factor kappa-B ligand (RANKL)-induced osteoclastogenesis by regulating the expression of anti-osteoclastic genes. However, while the vitamin D protective functions in OP and Pso have been definitively ascertained, the overall effect of IL-33 on bone and skin homeostasis, because of its pleiotropic action, is still controversial. Emerging evidence suggests a functional link between vitamin D and the IL-33/ST2 axis, which acts through hormonal influences and immune-mediated effects, as well as cellular and metabolic functions. Based on the actions of vitamin D and IL-33 in Pso and OP, here, we hypothesize the role of their crosstalk in the pathogenesis of both these pathologies.

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“…Dysregulated autophagy is involved in several pathological processes [41], including psoriasis, where autophagy deficiency leads to inflammatory cytokine production and cell proliferation in keratinocytes (KCs) [42], while inhibitors of autophagy may have beneficial effects on osteoporosis [43]. Moreover, medications that are used to treat psoriasis such as glucocorticoids and cyclosporine are known to affect bone density [44,45].…”

Section: Psoriasismentioning

confidence: 99%

Osteoporosis in Skin Diseases

Sirufo

Pietro

Bassino

et al. 2020

IJMS

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Osteoporosis (OP) is defined as a generalized skeletal disease characterized by low bone mass and an alteration of the microarchitecture that lead to an increase in bone fragility and, therefore, an increased risk of fractures. It must be considered today as a true public health problem and the most widespread metabolic bone disease that affects more than 200 million people worldwide. Under physiological conditions, there is a balance between bone formation and bone resorption necessary for skeletal homeostasis. In pathological situations, this balance is altered in favor of osteoclast (OC)-mediated bone resorption. During chronic inflammation, the balance between bone formation and bone resorption may be considerably affected, contributing to a net prevalence of osteoclastogenesis. Skin diseases are the fourth cause of human disease in the world, affecting approximately one third of the world’s population with a prevalence in elderly men. Inflammation and the various associated cytokine patterns are the basis of both osteoporosis and most skin pathologies. Moreover, dermatological patients also undergo local or systemic treatments with glucocorticoids and immunosuppressants that could increase the risk of osteoporosis. Therefore, particular attention should be paid to bone health in these patients. The purpose of the present review is to take stock of the knowledge in this still quite unexplored field, despite the frequency of such conditions in clinical practice.

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Autophagy in Skin Diseases

Cited by 50 publications

References 120 publications

Assessment of the Effect of Metabolic Syndrome on the Autophagy Marker LC3 in Psoriasis Vulgaris Patients: A Cross-Sectional Study

Assessment of the Effect of Metabolic Syndrome on the Autophagy Marker LC3 in Psoriasis Vulgaris Patients: A Cross-Sectional Study

IL-33/Vitamin D Crosstalk in Psoriasis-Associated Osteoporosis

Osteoporosis in Skin Diseases

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