Transcriptomic study on Psoriasis

[Fred]

Could psoriasis flares be linked to cellular energy and mitochondria?

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Background:
Psoriasis is an immune-mediated inflammatory disease driven by dysregulated crosstalk between immune cells and skin-resident cell populations, particularly keratinocytes and fibroblasts. However, transcriptomic findings across studies remain heterogeneous and incompletely integrated.

Objectives:
To integrate transcriptomic evidence across independent studies to define reproducible immune-gene expression patterns in plaque psoriasis and identify hypothesis-generating pathways beyond canonical immune programmes.

Methods:
We performed a systematic review and meta-analysis of transcriptomic datasets comparing lesional psoriatic skin with non-lesional skin and healthy controls. All analyses were restricted a priori to a curated set of immune-related genes. Forty-four independent studies comprising 975 samples were harmonized; differential expression within each study was combined using random-effects models. Functional enrichment (Reactome/KEGG/GO) and a systematic comparison with curated resources were conducted.

Results:
The meta-analysis identified 1780 immune-related genes consistently dysregulated in lesional psoriasis. Enrichment confirmed established immune programmes (e.g. IL-23/Th17 signalling, cytokine-mediated responses and type I interferon pathways). When cross-referenced with curated disease–gene resources, 1119 genes overlapped with previously reported psoriasis-associated genes, whereas 661 genes were not systematically highlighted. Exploratory enrichment among the less-characterized genes suggested additional processes involving glucose metabolism (gluconeogenesis), FoxO signalling and mitophagy, each supported by small gene sets and borderline adjusted p-values, and therefore interpreted as hypothesis-generating rather than definitive.

Conclusions:
By integrating 44 datasets under an explicit immune-gene framework, this study refines consensus immune signatures in psoriasis and prioritizes metabolic and mitochondrial processes as testable hypotheses for future functional work. These findings contextualize expected immune activation and point to potential interfaces between immunity, cellular energetics and mitochondrial quality control in lesional skin.

Source: onlinelibrary.wiley.com

*Funding: Ministerio de Ciencia, Innovación y Universidades. Conselleria d'Educació, Investigació, Cultura i Esport. Instituto de Salud Carlos III.

[Caroline]

Could psoriasis flares be linked to cellular energy and mitochondria?

Quote:

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Background:
Psoriasis is an immune-mediated inflammatory disease driven by dysregulated crosstalk between immune cells and skin-resident cell populations, particularly keratinocytes and fibroblasts. However, transcriptomic findings across studies remain heterogeneous and incompletely integrated.

Objectives:
To integrate transcriptomic evidence across independent studies to define reproducible immune-gene expression patterns in plaque psoriasis and identify hypothesis-generating pathways beyond canonical immune programmes.

Methods:
We performed a systematic review and meta-analysis of transcriptomic datasets comparing lesional psoriatic skin with non-lesional skin and healthy controls. All analyses were restricted a priori to a curated set of immune-related genes. Forty-four independent studies comprising 975 samples were harmonized; differential expression within each study was combined using random-effects models. Functional enrichment (Reactome/KEGG/GO) and a systematic comparison with curated resources were conducted.

Results:
The meta-analysis identified 1780 immune-related genes consistently dysregulated in lesional psoriasis. Enrichment confirmed established immune programmes (e.g. IL-23/Th17 signalling, cytokine-mediated responses and type I interferon pathways). When cross-referenced with curated disease–gene resources, 1119 genes overlapped with previously reported psoriasis-associated genes, whereas 661 genes were not systematically highlighted. Exploratory enrichment among the less-characterized genes suggested additional processes involving glucose metabolism (gluconeogenesis), FoxO signalling and mitophagy, each supported by small gene sets and borderline adjusted p-values, and therefore interpreted as hypothesis-generating rather than definitive.

Conclusions:
By integrating 44 datasets under an explicit immune-gene framework, this study refines consensus immune signatures in psoriasis and prioritizes metabolic and mitochondrial processes as testable hypotheses for future functional work. These findings contextualize expected immune activation and point to potential interfaces between immunity, cellular energetics and mitochondrial quality control in lesional skin.

Source: onlinelibrary.wiley.com

*Funding: Ministerio de Ciencia, Innovación y Universidades. Conselleria d'Educació, Investigació, Cultura i Esport. Instituto de Salud Carlos III.

I really do believe in the approach towards mitochondrial influence.
That would completely explain why people like Alan have success with their approach through food adaptation. There is also a tendency in the Netherlands, to take a good look at lifestyle in case of psoriasis.
Why food? Well, mitochondria are the energy cells in our body, and how can they fulfill their purpose … only if they are able to take up the results of digested food.