FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2801876219> ?p ?o ?g. }

• W2801876219 endingPage "e121" @default.
• W2801876219 startingPage "e121" @default.
• W2801876219 abstract "To the Editor: The results of the recent meta-analysis by Bui et al have confirmed that hidradenitis suppurativa (HS) is significantly associated with an increased prevalence of type 2 diabetes mellitus (T2DM).1Bui T.L. Silva-Hirschberg C. Torres J. et al.Hidradenitis suppurativa and diabetes mellitus: a systematic review and meta-analysis.J Am Acad Dermatol. 2017; 78: 395-402Abstract Full Text Full Text PDF PubMed Scopus (25) Google Scholar According to the authors, this association could be due to the fact that HS patients tend to be more obese.1Bui T.L. Silva-Hirschberg C. Torres J. et al.Hidradenitis suppurativa and diabetes mellitus: a systematic review and meta-analysis.J Am Acad Dermatol. 2017; 78: 395-402Abstract Full Text Full Text PDF PubMed Scopus (25) Google Scholar In this regard, we think that altered mechanistic target of rapamycin complex 1 (mTORC1) signaling might contribute and explain the connection between HS and T2DM. mTOR is the core constituent of the phosphatidylinositol 3-kinase–related kinase protein family that forms at least 2 multiprotein complexes known as mTORC1 and mTORC2.2Blagosklonny M.V. TOR-centric view on insulin resistance and diabetic complications: perspective for endocrinologists and gerontologists.Cell Death Dis. 2013; 4: e964Crossref PubMed Scopus (95) Google Scholar mTORC1 is the major regulator of survival, growth, proliferation, and motility in response to mitogens, energy, and nutrient levels. Because of its central role in cellular functions, mTORC1 dysregulation is involved in a large number of diseases.2Blagosklonny M.V. TOR-centric view on insulin resistance and diabetic complications: perspective for endocrinologists and gerontologists.Cell Death Dis. 2013; 4: e964Crossref PubMed Scopus (95) Google Scholar Upregulation of mTORC1 has also been observed in common inflammatory dermatoses, such as psoriasis and HS.3Monfrecola G. Balato A. Caiazzo G. et al.Mammalian target of rapamycin, insulin resistance and hidradenitis suppurativa: a possible metabolic loop.J Eur Acad Dermatol Venereol. 2016; 30: 1631-1633Crossref PubMed Scopus (42) Google Scholar Interestingly, mTORC1 plays a key role in diabetes mellitus pathogenesis.2Blagosklonny M.V. TOR-centric view on insulin resistance and diabetic complications: perspective for endocrinologists and gerontologists.Cell Death Dis. 2013; 4: e964Crossref PubMed Scopus (95) Google Scholar Overactivated mTORC1 causes insulin resistance. First, mTORC1 activates S6 kinase, which in turn causes phosphorylation and degradation of insulin receptor substrate 1/2. This impairs insulin signaling. Second, mTORC1 causes insulin resistance by affecting growth factor receptor–bound protein 10. Thus, hyperactivation of mTORC1 causes insulin resistance by at least 2 mechanisms.2Blagosklonny M.V. TOR-centric view on insulin resistance and diabetic complications: perspective for endocrinologists and gerontologists.Cell Death Dis. 2013; 4: e964Crossref PubMed Scopus (95) Google Scholar Glucose activates mTORC1, thus causing expansion and hypertrophy of beta cells and increasing insulin secretion. Initially, this hyperfunction of beta cells compensates for insulin resistance, preventing hyperglycemia. However, it is hyperfunction that eventually causes beta-cell failure and manifests as diabetes. In fact, chronic hyperstimulation of mTORC1 renders beta cells resistant to insulin-like growth factor 1 and insulin, fostering cell death.2Blagosklonny M.V. TOR-centric view on insulin resistance and diabetic complications: perspective for endocrinologists and gerontologists.Cell Death Dis. 2013; 4: e964Crossref PubMed Scopus (95) Google Scholar Furthermore, the mTORC1 pathway is of pivotal importance for metabolic regulation and functioning of innate and adaptive immune cells, as clearly verified by the immune-suppressive function of mTORC1 inhibitors such as rapamycin. Notably, the differentiation of T helper 17 (TH17) cells is controlled and promoted by mTORC1.4De Vita V. Melnik B.C. The magnitude of mTORC1 signalling may predict the response to isotretinoin treatment in patients with hidradenitis suppurativa.Dermatology. 2017; 233: 399-400Crossref PubMed Scopus (6) Google Scholar Substantial infiltration of TH17 cells into lesional skin and increased IL-17 serum levels have been found in HS patients.5Matusiak Ł. Szczęch J. Bieniek A. et al.Increased interleukin (IL)-17 serum levels in patients with hidradenitis suppurativa: implications for treatment with anti-IL-17 agents.J Am Acad Dermatol. 2017; 76: 670-675Abstract Full Text Full Text PDF PubMed Scopus (105) Google Scholar Evidence shows that interleukin (IL)-17 also plays a key role in insulin resistance and diabetes mellitus.6Owczarczyk-Saczonek A. Placek W. Interleukin-17 as a factor linking the pathogenesis of psoriasis with metabolic disorders.Int J Dermatol. 2017; 56: 260-268Crossref PubMed Scopus (26) Google Scholar Obesity is one of the main known causes of the development of T2DM. In obese patients, increased plasma concentrations of insulin, insulin-like growth factor 1, and IL-17 are observed.6Owczarczyk-Saczonek A. Placek W. Interleukin-17 as a factor linking the pathogenesis of psoriasis with metabolic disorders.Int J Dermatol. 2017; 56: 260-268Crossref PubMed Scopus (26) Google Scholar Serum IL-17 is significantly higher in patients with T2DM than in controls. IL-17 deficiency increased glucose tolerance and sensitivity to insulin in young mice.6Owczarczyk-Saczonek A. Placek W. Interleukin-17 as a factor linking the pathogenesis of psoriasis with metabolic disorders.Int J Dermatol. 2017; 56: 260-268Crossref PubMed Scopus (26) Google Scholar Expression levels of tumor necrosis factor (TNF) alpha in lesional skin and serum are increased in HS. TNF-alpha activates the kinase IKKβ, which inactivates hamartin, a key negative regulator of mTORC1. Thus, TNF-alfa impairs insulin signaling and contributes to insulin resistance. Anti–TNF-alpha therapies, such as adalimumab, decrease mTORC1 activity and improve insulin sensitivity. Metformin, a drug that reduces insulin resistance, has been identified as an mTORC1 inhibitor and attenuates psoriasis vulgaris and HS.4De Vita V. Melnik B.C. The magnitude of mTORC1 signalling may predict the response to isotretinoin treatment in patients with hidradenitis suppurativa.Dermatology. 2017; 233: 399-400Crossref PubMed Scopus (6) Google Scholar In summary, evidence suggests that HS and T2DM share a common pathogenic substrate, namely hyperactivated mTORC1 signaling. Hidradenitis suppurativa and diabetes mellitus: A systematic review and meta-analysisJournal of the American Academy of DermatologyVol. 78Issue 2PreviewThe relationship between hidradenitis suppurativa and diabetes mellitus is not well understood. Full-Text PDF" @default.
• W2801876219 created "2018-05-17" @default.
• W2801876219 creator A5014420805 @default.
• W2801876219 creator A5047969702 @default.
• W2801876219 date "2018-05-01" @default.
• W2801876219 modified "2023-09-23" @default.
• W2801876219 title "Activated mTORC1 signaling: The common driving force of type 2 diabetes and hidradenitis suppurativa" @default.
• W2801876219 cites W1957680909 @default.
• W2801876219 cites W2031585142 @default.
• W2801876219 cites W2529762632 @default.
• W2801876219 cites W2564885013 @default.
• W2801876219 cites W2766558895 @default.
• W2801876219 cites W2781003619 @default.
• W2801876219 doi "https://doi.org/10.1016/j.jaad.2017.11.061" @default.
• W2801876219 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/29678383" @default.
• W2801876219 hasPublicationYear "2018" @default.
• W2801876219 type Work @default.
• W2801876219 sameAs 2801876219 @default.
• W2801876219 citedByCount "12" @default.
• W2801876219 countsByYear W28018762192018 @default.
• W2801876219 countsByYear W28018762192019 @default.
• W2801876219 countsByYear W28018762192020 @default.
• W2801876219 countsByYear W28018762192022 @default.
• W2801876219 countsByYear W28018762192023 @default.
• W2801876219 crossrefType "journal-article" @default.
• W2801876219 hasAuthorship W2801876219A5014420805 @default.
• W2801876219 hasAuthorship W2801876219A5047969702 @default.
• W2801876219 hasBestOaLocation W28018762191 @default.
• W2801876219 hasConcept C126322002 @default.
• W2801876219 hasConcept C134018914 @default.
• W2801876219 hasConcept C2776002364 @default.
• W2801876219 hasConcept C2777180221 @default.
• W2801876219 hasConcept C2777391703 @default.
• W2801876219 hasConcept C2777949483 @default.
• W2801876219 hasConcept C2779134260 @default.
• W2801876219 hasConcept C54355233 @default.
• W2801876219 hasConcept C555293320 @default.
• W2801876219 hasConcept C60644358 @default.
• W2801876219 hasConcept C62478195 @default.
• W2801876219 hasConcept C71924100 @default.
• W2801876219 hasConcept C86554907 @default.
• W2801876219 hasConcept C86803240 @default.
• W2801876219 hasConcept C98490376 @default.
• W2801876219 hasConceptScore W2801876219C126322002 @default.
• W2801876219 hasConceptScore W2801876219C134018914 @default.
• W2801876219 hasConceptScore W2801876219C2776002364 @default.
• W2801876219 hasConceptScore W2801876219C2777180221 @default.
• W2801876219 hasConceptScore W2801876219C2777391703 @default.
• W2801876219 hasConceptScore W2801876219C2777949483 @default.
• W2801876219 hasConceptScore W2801876219C2779134260 @default.
• W2801876219 hasConceptScore W2801876219C54355233 @default.
• W2801876219 hasConceptScore W2801876219C555293320 @default.
• W2801876219 hasConceptScore W2801876219C60644358 @default.
• W2801876219 hasConceptScore W2801876219C62478195 @default.
• W2801876219 hasConceptScore W2801876219C71924100 @default.
• W2801876219 hasConceptScore W2801876219C86554907 @default.
• W2801876219 hasConceptScore W2801876219C86803240 @default.
• W2801876219 hasConceptScore W2801876219C98490376 @default.
• W2801876219 hasIssue "5" @default.
• W2801876219 hasLocation W28018762191 @default.
• W2801876219 hasLocation W28018762192 @default.
• W2801876219 hasOpenAccess W2801876219 @default.
• W2801876219 hasPrimaryLocation W28018762191 @default.
• W2801876219 hasRelatedWork W1488655057 @default.
• W2801876219 hasRelatedWork W2054117275 @default.
• W2801876219 hasRelatedWork W2078821200 @default.
• W2801876219 hasRelatedWork W2120435825 @default.
• W2801876219 hasRelatedWork W2131978771 @default.
• W2801876219 hasRelatedWork W2550775385 @default.
• W2801876219 hasRelatedWork W2774620560 @default.
• W2801876219 hasRelatedWork W2943393881 @default.
• W2801876219 hasRelatedWork W2973141720 @default.
• W2801876219 hasRelatedWork W3185746211 @default.
• W2801876219 hasVolume "78" @default.
• W2801876219 isParatext "false" @default.
• W2801876219 isRetracted "false" @default.
• W2801876219 magId "2801876219" @default.
• W2801876219 workType "article" @default.