Investigating Transcriptional Age Acceleration in Inflammatory Skin Diseases
Epigenetic age acceleration has previously been observed in inflammatory skin disease; however, less is known regarding recently described age-related gene expression patterns (“transcriptional clocks”). We investigated the role of transcriptional clocks in patients with hidradenitis suppurativa (n...
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| Published in | JID innovations Vol. 5; no. 5; p. 100386 |
|---|---|
| Main Authors | , , , , , , , , |
| Format | Journal Article |
| Language | English |
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Netherlands
Elsevier Inc
01.09.2025
Elsevier |
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| Online Access | Get full text |
| ISSN | 2667-0267 2667-0267 |
| DOI | 10.1016/j.xjidi.2025.100386 |
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| Abstract | Epigenetic age acceleration has previously been observed in inflammatory skin disease; however, less is known regarding recently described age-related gene expression patterns (“transcriptional clocks”). We investigated the role of transcriptional clocks in patients with hidradenitis suppurativa (n = 37), those with atopic dermatitis (n = 27), those with plaque psoriasis (n = 28), and healthy subjects (n = 38) using 7 clock algorithms, to improve the understanding of underlying pathophysiology and disease trajectory. Five of 7 transcriptional clocks demonstrated moderate-to-strong accuracy in predicting age across groups (patients with atopic dermatitis: ρ = 0.40–0.86, those with hidradenitis suppurativa: ρ = 0.46–0.74, those with plaque psoriasis: ρ = 0.50–0.80, healthy subjects: ρ = 0.32–0.60; P < .05). Age acceleration was observed in lesional versus healthy (patients with atopic dermatitis: +3.9∼9.8y, t = 2.8∼5.9; those with hidradenitis suppurativa: +5.0∼6.1y, t = 2.5∼4.1; those with plaque psoriasis: +6.5∼12.5y, t = 5.1∼8.0; P < .05) and in lesional versus nonlesional skin in all diseases and less frequently observed in nonlesional versus healthy skin. In atopic dermatitis, loss-of-function sequence variants in the FLG gene were associated with transcriptional age acceleration, including FLGR244X/2282del4 dual carrier status (t = 2.3, P < .05) and FLGR501X carrier status (t = 2.6, P < .05). Pathway enrichment analyses revealed that clock genes are enriched in signatures related to aging, inflammation, and metabolism. Our study provides evidence for transcriptional age acceleration in inflammatory skin disease and sets a foundation for further investigation into the role of age-related transcriptional changes in the pathophysiology of these diseases. |
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| AbstractList | Epigenetic age acceleration has previously been observed in inflammatory skin disease; however, less is known regarding recently described age-related gene expression patterns (“transcriptional clocks”). We investigated the role of transcriptional clocks in patients with hidradenitis suppurativa (n = 37), those with atopic dermatitis (n = 27), those with plaque psoriasis (n = 28), and healthy subjects (n = 38) using 7 clock algorithms, to improve the understanding of underlying pathophysiology and disease trajectory. Five of 7 transcriptional clocks demonstrated moderate-to-strong accuracy in predicting age across groups (patients with atopic dermatitis:
ρ
= 0.40–0.86, those with hidradenitis suppurativa:
ρ
= 0.46–0.74, those with plaque psoriasis:
ρ
= 0.50–0.80, healthy subjects:
ρ
= 0.32–0.60;
P
< .05). Age acceleration was observed in lesional versus healthy (patients with atopic dermatitis: +3.9∼9.8y,
t =
2.8∼5.9; those with hidradenitis suppurativa: +5.0∼6.1y,
t
= 2.5∼4.1; those with plaque psoriasis: +6.5∼12.5y,
t
= 5.1∼8.0;
P
< .05) and in lesional versus nonlesional skin in all diseases and less frequently observed in nonlesional versus healthy skin. In atopic dermatitis, loss-of-function sequence variants in the FLG gene were associated with transcriptional age acceleration, including
FLGR244X/2282del4
dual carrier status (
t
= 2.3,
P
< .05) and
FLGR501X
carrier status (
t
= 2.6,
P
< .05). Pathway enrichment analyses revealed that clock genes are enriched in signatures related to aging, inflammation, and metabolism. Our study provides evidence for transcriptional age acceleration in inflammatory skin disease and sets a foundation for further investigation into the role of age-related transcriptional changes in the pathophysiology of these diseases. Epigenetic age acceleration has previously been observed in inflammatory skin disease; however, less is known regarding recently described age-related gene expression patterns (“transcriptional clocks”). We investigated the role of transcriptional clocks in patients with hidradenitis suppurativa (n = 37), those with atopic dermatitis (n = 27), those with plaque psoriasis (n = 28), and healthy subjects (n = 38) using 7 clock algorithms, to improve the understanding of underlying pathophysiology and disease trajectory. Five of 7 transcriptional clocks demonstrated moderate-to-strong accuracy in predicting age across groups (patients with atopic dermatitis: ρ = 0.40–0.86, those with hidradenitis suppurativa: ρ = 0.46–0.74, those with plaque psoriasis: ρ = 0.50–0.80, healthy subjects: ρ = 0.32–0.60; P < .05). Age acceleration was observed in lesional versus healthy (patients with atopic dermatitis: +3.9∼9.8y, t = 2.8∼5.9; those with hidradenitis suppurativa: +5.0∼6.1y, t = 2.5∼4.1; those with plaque psoriasis: +6.5∼12.5y, t = 5.1∼8.0; P < .05) and in lesional versus nonlesional skin in all diseases and less frequently observed in nonlesional versus healthy skin. In atopic dermatitis, loss-of-function sequence variants in the FLG gene were associated with transcriptional age acceleration, including FLGR244X/2282del4 dual carrier status (t = 2.3, P < .05) and FLGR501X carrier status (t = 2.6, P < .05). Pathway enrichment analyses revealed that clock genes are enriched in signatures related to aging, inflammation, and metabolism. Our study provides evidence for transcriptional age acceleration in inflammatory skin disease and sets a foundation for further investigation into the role of age-related transcriptional changes in the pathophysiology of these diseases. Epigenetic age acceleration has previously been observed in inflammatory skin disease; however, less is known regarding recently described age-related gene expression patterns ("transcriptional clocks"). We investigated the role of transcriptional clocks in patients with hidradenitis suppurativa (n = 37), those with atopic dermatitis (n = 27), those with plaque psoriasis (n = 28), and healthy subjects (n = 38) using 7 clock algorithms, to improve the understanding of underlying pathophysiology and disease trajectory. Five of 7 transcriptional clocks demonstrated moderate-to-strong accuracy in predicting age across groups (patients with atopic dermatitis: ρ = 0.40-0.86, those with hidradenitis suppurativa: ρ = 0.46-0.74, those with plaque psoriasis: ρ = 0.50-0.80, healthy subjects: ρ = 0.32-0.60; P < .05). Age acceleration was observed in lesional versus healthy (patients with atopic dermatitis: +3.9∼9.8y, t = 2.8∼5.9; those with hidradenitis suppurativa: +5.0∼6.1y, t = 2.5∼4.1; those with plaque psoriasis: +6.5∼12.5y, t = 5.1∼8.0; P < .05) and in lesional versus nonlesional skin in all diseases and less frequently observed in nonlesional versus healthy skin. In atopic dermatitis, loss-of-function sequence variants in the FLG gene were associated with transcriptional age acceleration, including FLGR244X/2282del4 dual carrier status (t = 2.3, P < .05) and FLGR501X carrier status (t = 2.6, P < .05). Pathway enrichment analyses revealed that clock genes are enriched in signatures related to aging, inflammation, and metabolism. Our study provides evidence for transcriptional age acceleration in inflammatory skin disease and sets a foundation for further investigation into the role of age-related transcriptional changes in the pathophysiology of these diseases.Epigenetic age acceleration has previously been observed in inflammatory skin disease; however, less is known regarding recently described age-related gene expression patterns ("transcriptional clocks"). We investigated the role of transcriptional clocks in patients with hidradenitis suppurativa (n = 37), those with atopic dermatitis (n = 27), those with plaque psoriasis (n = 28), and healthy subjects (n = 38) using 7 clock algorithms, to improve the understanding of underlying pathophysiology and disease trajectory. Five of 7 transcriptional clocks demonstrated moderate-to-strong accuracy in predicting age across groups (patients with atopic dermatitis: ρ = 0.40-0.86, those with hidradenitis suppurativa: ρ = 0.46-0.74, those with plaque psoriasis: ρ = 0.50-0.80, healthy subjects: ρ = 0.32-0.60; P < .05). Age acceleration was observed in lesional versus healthy (patients with atopic dermatitis: +3.9∼9.8y, t = 2.8∼5.9; those with hidradenitis suppurativa: +5.0∼6.1y, t = 2.5∼4.1; those with plaque psoriasis: +6.5∼12.5y, t = 5.1∼8.0; P < .05) and in lesional versus nonlesional skin in all diseases and less frequently observed in nonlesional versus healthy skin. In atopic dermatitis, loss-of-function sequence variants in the FLG gene were associated with transcriptional age acceleration, including FLGR244X/2282del4 dual carrier status (t = 2.3, P < .05) and FLGR501X carrier status (t = 2.6, P < .05). Pathway enrichment analyses revealed that clock genes are enriched in signatures related to aging, inflammation, and metabolism. Our study provides evidence for transcriptional age acceleration in inflammatory skin disease and sets a foundation for further investigation into the role of age-related transcriptional changes in the pathophysiology of these diseases. Epigenetic age acceleration has previously been observed in inflammatory skin disease; however, less is known regarding recently described age-related gene expression patterns ("transcriptional clocks"). We investigated the role of transcriptional clocks in patients with hidradenitis suppurativa (n = 37), those with atopic dermatitis (n = 27), those with plaque psoriasis (n = 28), and healthy subjects (n = 38) using 7 clock algorithms, to improve the understanding of underlying pathophysiology and disease trajectory. Five of 7 transcriptional clocks demonstrated moderate-to-strong accuracy in predicting age across groups (patients with atopic dermatitis: = 0.40-0.86, those with hidradenitis suppurativa: = 0.46-0.74, those with plaque psoriasis: = 0.50-0.80, healthy subjects: = 0.32-0.60; < .05). Age acceleration was observed in lesional versus healthy (patients with atopic dermatitis: +3.9∼9.8y, 2.8∼5.9; those with hidradenitis suppurativa: +5.0∼6.1y, = 2.5∼4.1; those with plaque psoriasis: +6.5∼12.5y, = 5.1∼8.0; < .05) and in lesional versus nonlesional skin in all diseases and less frequently observed in nonlesional versus healthy skin. In atopic dermatitis, loss-of-function sequence variants in the FLG gene were associated with transcriptional age acceleration, including dual carrier status ( = 2.3, < .05) and carrier status ( = 2.6, < .05). Pathway enrichment analyses revealed that clock genes are enriched in signatures related to aging, inflammation, and metabolism. Our study provides evidence for transcriptional age acceleration in inflammatory skin disease and sets a foundation for further investigation into the role of age-related transcriptional changes in the pathophysiology of these diseases. |
| ArticleNumber | 100386 |
| Author | Caucheteux, Stephan Galati, Melissa Li, Kaiyang Piguet, Vincent Jeremian, Richie Croitoru, David O. Fotovati, Rayyan Lefrançois, Philippe Jack, Carolyn |
| Author_xml | – sequence: 1 givenname: Richie orcidid: 0000-0001-9258-6296 surname: Jeremian fullname: Jeremian, Richie organization: Division of Dermatology, Department of Medicine, McGill University, Montréal, Canada – sequence: 2 givenname: Melissa orcidid: 0009-0005-3034-5725 surname: Galati fullname: Galati, Melissa organization: Temerty Faculty of Medicine, University of Toronto, Toronto, Canada – sequence: 3 givenname: Rayyan orcidid: 0009-0000-4392-4869 surname: Fotovati fullname: Fotovati, Rayyan organization: Faculty of Medicine and Health Sciences, McGill University, Montréal, Canada – sequence: 4 givenname: Kaiyang orcidid: 0000-0001-8557-166X surname: Li fullname: Li, Kaiyang organization: Faculty of Medicine and Health Sciences, McGill University, Montréal, Canada – sequence: 5 givenname: Carolyn orcidid: 0000-0002-0376-3324 surname: Jack fullname: Jack, Carolyn organization: Division of Dermatology, Department of Medicine, McGill University, Montréal, Canada – sequence: 6 givenname: David O. orcidid: 0000-0003-4637-2291 surname: Croitoru fullname: Croitoru, David O. organization: Division of Dermatology, Department of Medicine, Temerty Faculty of Medicine, University of Toronto, Toronto, Canada – sequence: 7 givenname: Stephan orcidid: 0000-0003-1373-1331 surname: Caucheteux fullname: Caucheteux, Stephan organization: Division of Dermatology, Department of Medicine, Temerty Faculty of Medicine, University of Toronto, Toronto, Canada – sequence: 8 givenname: Philippe orcidid: 0000-0003-2939-7956 surname: Lefrançois fullname: Lefrançois, Philippe organization: Lady Davis Institute (LDI), Jewish General Hospital, Montréal, Canada – sequence: 9 givenname: Vincent orcidid: 0000-0001-6079-4517 surname: Piguet fullname: Piguet, Vincent email: vincent.piguet@utoronto.ca organization: Division of Dermatology, Department of Medicine, Temerty Faculty of Medicine, University of Toronto, Toronto, Canada |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/40727671$$D View this record in MEDLINE/PubMed |
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| Keywords | PP AD Hidradenitis suppurativa Psoriasis RNA-seq Atopic dermatitis CI Aging GO HS plaque psoriasis confidence interval Gene Ontology |
| Language | English |
| License | This is an open access article under the CC BY-NC-ND license. 2025 Published by Elsevier Inc. on behalf of the Society for Investigative Dermatology. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/). |
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