Potential Therapeutic Approaches through Modulating the Autophagy Process for Skin Barrier Dysfunction

Choi, Min Sik; Chae, Yoon-Jee; Choi, Ji Woong; Chang, Ji‐Eun

doi:10.3390/ijms22157869

Cited by 11 publications

(6 citation statements)

References 126 publications

(133 reference statements)

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“…Autophagy plays a substantial role in the homeostasis of skin development. Loss or impairment of autophagy has been associated with a number of skin conditions (50). For instance, the downregulation of LC3 (51) and the upregulation of p62 (52), which reflect a blockage of autophagy, are involved in inflammation in psoriasis; likewise, the autophagy activator rapamycin alleviates imiquimod-induced psoriasis-like dermatitis (51).…”

Section: Discussionmentioning

confidence: 99%

Human β-defensin-3 attenuates atopic dermatitis–like inflammation through autophagy activation and the aryl hydrocarbon receptor signaling pathway

Peng¹,

Tsukamoto²,

Ikutama³

et al. 2022

Journal of Clinical Investigation

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Human β-defensin (hBD)-3 exhibits antimicrobial and immunomodulatory activities; however, its contribution to autophagy regulation remains unclear, and the role of autophagy in the regulation of the epidermal barrier in atopic dermatitis (AD) is poorly understood. Here, keratinocyte autophagy was restrained in the skin lesions of patients with AD and murine models of AD.Interestingly, hBD-3 alleviated the interleukin-4-and interleukin-13-mediated impairment of the tight junction (TJ) barrier through keratinocyte autophagy activation, which involved aryl hydrocarbon receptor (AhR) signaling. While autophagy deficiency impaired the epidermal barrier and exacerbated inflammation, hBD-3 attenuated skin inflammation and enhanced the TJ barrier in AD. Importantly, hBD-3-mediated improvement of the TJ barrier was abolished in autophagydeficient AD mice and in AhR-suppressed AD mice, suggesting a role for hBD-3-mediated autophagy in the regulation of the epidermal barrier and inflammation in AD. Thus, autophagy contributes to the pathogenesis of AD, and hBD-3 could be used for therapeutic purposes.

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Section: Discussionmentioning

confidence: 99%

Human β-defensin-3 attenuates atopic dermatitis–like inflammation through autophagy activation and the aryl hydrocarbon receptor signaling pathway

Peng¹,

Tsukamoto²,

Ikutama³

et al. 2022

Journal of Clinical Investigation

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“…Autophagy is essential for skin homeostasis. The dysfunctional regulation of autophagy responses leads to several skin disorders, including psoriasis [ 13 , 14 ]. LC3 and p62 are two well-characterized autophagy biomarkers used to represent and quantify the status of autophagy [ 13 , 14 , 15 ].…”

Section: Discussionmentioning

confidence: 99%

“…The dysfunctional regulation of autophagy responses leads to several skin disorders, including psoriasis [ 13 , 14 ]. LC3 and p62 are two well-characterized autophagy biomarkers used to represent and quantify the status of autophagy [ 13 , 14 , 15 ]. Previous studies reported that LC3B protein expression was lower in psoriatic lesional skin than in non-lesional skin [ 16 , 17 ].…”

Section: Discussionmentioning

confidence: 99%

Lithosepermic Acid Restored the Skin Barrier Functions in the Imiquimod-Induced Psoriasis-like Animal Model

Chen

Cheng

Liu

et al. 2022

IJMS

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(1) Background: Psoriasis is a T helper 1/T helper 17 cells-involved immune-mediated genetic disease. Lithospermic acid, one of the major phenolic acid compounds of Danshen, has antioxidation and anti-inflammation abilities. Due to the inappropriate molecular weight for topical penetration through the stratum corneum, lithospermic acid was loaded into the well-developed microemulsion delivery system for IMQ-induced psoriasis-like dermatitis treatment. (2) Methods: BALB/c mice were administered with topical imiquimod to induce psoriasis-like dermatitis. Skin barrier function, disease severity, histology assessment, autophagy-related protein expression, and skin and spleen cytokine expression were evaluated. (3) Results: The morphology, histopathology, and skin barrier function results showed that 0.1% lithospermic acid treatment ameliorated the IMQ-induced psoriasis-like dermatitis and restored the skin barrier function. The cytokines array results confirmed that 0.1% lithospermic acid treatment inhibited the cutaneous T helper-17/Interleukin-23 axis related cytokines cascades. (4) Conclusions: The results implied that lithospermic acid might represent a possible new therapeutic agent for psoriasis treatment.

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“…In addition, autophagy may also regulate key inflammatory cytokines in tumors. Accordingly, autophagy leads to opposing consequences for the tumor since it works as both a tumor suppressor and a tumor promotor [ 13 ]. Figure 2 represents autophagy signaling pathways involved in cancer-associated inflammation.…”

Section: Introductionmentioning

confidence: 99%

Crosstalk between Autophagy and Inflammatory Processes in Cancer

Lee

Kim

Choi

et al. 2021

Life

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Inflammation is an adaptive response to tissue injury, which is a critical process in order to restore tissue functionality and homeostasis. The association between inflammation and cancer has been a topic of interest for many years, not only inflammatory cells themselves but also the chemokines and cytokines they produce, which affect cancer development. Autophagy is an intracellular self-degradative process providing elimination of damaged or dysfunctional organelles under stressful conditions such as nutrient deficiency, hypoxia, or chemotherapy. Interestingly, the signaling pathways that are involved in cancer-associated inflammation may regulate autophagy as well. These are 1) the toll-like receptor (TLR) signaling cascade, 2) the reactive oxygen species (ROS) signaling pathway, 3) the inflammatory cytokine signaling pathway, and 4) the IκB kinase (IKK)/Nuclear factor-κB (NF-κB) signaling axis. Moreover, the studies on the context-specific functions of autophagy during inflammatory responses in cancer will be discussed here. On that basis, we focus on autophagy inhibitors and activators regulating inflammatory process in cancer as useful candidates for enhancing anticancer effects. This review summarizes how the autophagic process regulates these key inflammatory processes and vice versa in various cancers.

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Potential Therapeutic Approaches through Modulating the Autophagy Process for Skin Barrier Dysfunction

Cited by 11 publications

References 126 publications

Human β-defensin-3 attenuates atopic dermatitis–like inflammation through autophagy activation and the aryl hydrocarbon receptor signaling pathway

Human β-defensin-3 attenuates atopic dermatitis–like inflammation through autophagy activation and the aryl hydrocarbon receptor signaling pathway

Lithosepermic Acid Restored the Skin Barrier Functions in the Imiquimod-Induced Psoriasis-like Animal Model

Crosstalk between Autophagy and Inflammatory Processes in Cancer

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