mTORC1 – a potential player in the pathogenesis of hidradenitis suppurativa?

Дмитриев, А.; König, Arne; Lang, Victoria; Diehl, Sandra; Kaufmann, Roland; Pinter, Andreas; Buerger, Claudia

doi:10.1111/jdv.17202

Cited by 7 publications

(12 citation statements)

References 10 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…60 Similarly, HS lesions show overlapping features with psoriatic skin inflammation, which could be because of the involvement of mTOR cascade in the pathogenesis of both. 61,62 PALANIVEL AND MILLINGTON Increased PI3K/AKT/mTOR signalling and resistance to apoptosis is found in basal cell carcinomas and cutaneous squamous cell carcinomas. 63,64 Activation of PI3K signalling can occur in keratinocytes stimulated by ultraviolet (UV) radiation and aberrant inflammatory cytokines.…”

Section: M-torc Signalling and Skin Inflammationmentioning

confidence: 99%

“…In a study using skin from hidradenitis suppurativa (HS) patients, there was increased expression of mTORC1 both on lesional and non‐lesional skin of HS patients 60 . Similarly, HS lesions show overlapping features with psoriatic skin inflammation, which could be because of the involvement of mTOR cascade in the pathogenesis of both 61, 62 …”

Section: M‐torc Signalling and Skin Inflammationmentioning

confidence: 99%

See 1 more Smart Citation

Obesity‐induced immunological effects on the skin

Palanivel¹,

Millington

2023

Skin Health and Disease

View full text Add to dashboard Cite

There is an increasing prevalence of obesity globally. Equally, the significance of maintaining a healthy body weight for maintaining a healthy skin homoeostasis is gaining greater attention. On this background, there is growing evidence of an adverse influence of excess body weight on the immune system, which has a resultant detrimental effect on the functioning of the skin. The presence of obesity appears to intensify various inflammatory skin disorders. These immune‐dermatological consequences in the obese occur because of multiple adverse changes in the skin physiology, endocrine imbalance, metabolic deviations, alterations in circulation, skin microbiome and immunological disruptions. The purpose of this article is to highlight the profound impact of increased fat deposition on cutaneous immunology and its role in the pathophysiology of various chronic inflammatory dermatological conditions. Understanding these immunological modulations will aid in developing therapies targeting the specific inflammatory mediators in the management of obesity‐associated chronic immunological skin disease.

show abstract

Section: M-torc Signalling and Skin Inflammationmentioning

confidence: 99%

Section: M‐torc Signalling and Skin Inflammationmentioning

confidence: 99%

Obesity‐induced immunological effects on the skin

Palanivel¹,

Millington

2023

Skin Health and Disease

View full text Add to dashboard Cite

show abstract

“…The production of IFN-γ and IL-17 is further supported by mTOR complex signaling, whose relevance might be deduced from the reported increased mTOR expression in HS lesions [81][82][83][84][85]. As previously reported by Schroder et al, IFN-γ induces Th1-attracting chemokines (e.g., CXCL10) and activates dermal endothelial cells, allowing the immune cell infiltration from the bloodstream [86].…”

Section: Main Cytokine Network In Hsmentioning

confidence: 56%

Hidradenitis Suppurativa: Where We Are and Where We Are Going

Scala

Cacciapuoti

Garzorz‐Stark

et al. 2021

Cells

View full text Add to dashboard Cite

Hidradenitis suppurativa (HS) is a chronic inflammatory skin disease primarily affecting apocrine gland-rich areas of the body. It is a multifactorial disease in which genetic and environmental factors play a key role. The primary defect in HS pathophysiology involves follicular occlusion of the folliculopilosebaceous unit, followed by follicular rupture and immune responses. Innate pro-inflammatory cytokines (e.g., IL-1β, and TNF-α); mediators of activated T helper (Th)1 and Th17 cells (e.g., IFN-γ, and IL-17); and effector mechanisms of neutrophilic granulocytes, macrophages, and plasma cells are involved. On the other hand, HS lesions contain anti-inflammatory mediators (e.g., IL-10) and show limited activity of Th22 cells. The inflammatory vicious circle finally results in pain, purulence, tissue destruction, and scarring. HS pathogenesis is still enigmatic, and a valid animal model for HS is currently not available. All these aspects represent a challenge for the development of therapeutic approaches, which are urgently needed for this debilitating disease. Available treatments are limited, mostly off-label, and surgical interventions are often required to achieve remission. In this paper, we provide an overview of the current knowledge surrounding HS, including the diagnosis, pathogenesis, treatments, and existing translational studies.

show abstract

“…Furthermore, pro‐inflammatory cytokines such as Interleukin (IL)‐1β, IL‐6, IL‐8, IL‐12, IL‐17, IL‐23, macrophage colony‐stimulating factor, interferon‐γ, tumour necrosis factor (TNF)‐α and anti‐inflammatory IL‐10 have been implicated to play an important role in the aberrant immune response of HS 12,13,15–17 . Besides, the inflammatory signalling pathways Notch, phosphoinositide‐3‐kinase/AKT, the inflammasome and the mechanistic target of rapamycin complex 1 show increased activity in HS 14,18,19 . Our limited understanding of the exact pathophysiological pathways contributing to the development and progression of HS, the treatment emphasizes the symptoms and the causes of the disease.…”

Section: Introductionmentioning

confidence: 99%

“…12,13,[15][16][17] Besides, the inflammatory signalling pathways Notch, phosphoinositide-3-kinase/AKT, the inflammasome and the mechanistic target of rapamycin complex 1 show increased activity in HS. 14,18,19 Our limited understanding of the exact pathophysiological pathways contributing to the development and progression of HS, the treatment emphasizes the symptoms and the causes of the disease. The German National and European S1 guideline for the treatment of HS as well as the North American clinical management guideline recommend the combination of the antibiotics clindamycin and rifampicin as first-line systemic therapy for moderate-to-severe forms of HS.…”

mentioning

confidence: 99%

Mechanism of anti‐inflammatory effects of rifampicin in an ex vivo culture system of hidradenitis suppurativa

Haferland

Wallenwein

Ickelsheimer

et al. 2022

Experimental Dermatology

View full text Add to dashboard Cite

Hidradenitis suppurativa (HS) is a chronic inflammatory skin disease caused by the obstruction of the hair follicle. It manifests in form of profound painful nodules and abscesses up to the formation of fistulas and sinus tracts. Areas involved in men and women are axillae, inguinal, gluteal and perianal whereby women can additionally be affected sub-mammary. 1 Many patients are smokers and suffer from comorbidities such as obesity, type 2-diabetes, chronic inflammatory bowel diseases and depression. This is associated with a considerable reduction of quality of life. 2,3 So far, the exact pathophysiological mechanisms underlying HS have not been understood completely. However, hyperkeratosis and perifolliculitis in the pilosebaceous-apocrine unit are assumed to precede the occlusion, inflammation and rupture of the hair follicle. [4][5][6] Subsequently, an increased inflammatory response due to the release of keratins,

show abstract

mTORC1 – a potential player in the pathogenesis of hidradenitis suppurativa?

Cited by 7 publications

References 10 publications

Obesity‐induced immunological effects on the skin

Obesity‐induced immunological effects on the skin

Hidradenitis Suppurativa: Where We Are and Where We Are Going

Mechanism of anti‐inflammatory effects of rifampicin in an ex vivo culture system of hidradenitis suppurativa

Contact Info

Product

Resources

About