ArticleJID innovations : skin science from molecules to population health2026
Spatial transcriptomic profiling reveals fibroblast and inflammatory signatures in calcinosis of chronic cutaneous lupus.
Article in JID innovations : skin science from molecules to population health, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Calcinosis cutis represents a debilitating complication of chronic cutaneous lupus erythematosus; however, its underlying molecular mechanisms remain poorly understood. We performed spatial transcriptomic profiling on skin biopsies from 4 patients with chronic cutaneous lupus erythematosus: 2 with calcinosis cutis and 2 without. Analysis of 87,730 cells across 6 major cell types revealed distinct molecular signatures associated with calcification. Fibroblasts in calcinosis cutis lesions exhibited significant upregulation of osteogenic and extracellular matrix genes, including periostin, collagen family members, and matrix metalloproteinase 2, accompanied by enrichment of pathways related to extracellular matrix organization and ossification. Endothelial cells demonstrated activation of hypoxia-responsive pathways, particularly hypoxia-inducible factor 2-alpha. Macrophages showed elevated chemokine receptor expression with corresponding ligand upregulation in endothelial cells, establishing a potential chemotactic recruitment axis. Spatial analysis revealed that these pathological features were concentrated in pericalcinosis regions, with reduced intercellular distances between functionally related cell populations. These findings demonstrate coordinated fibroblast osteogenic reprogramming, endothelial hypoxic responses, and immune cell activation within organized pericalcinosis niches. This spatial transcriptomic characterization of lupus-associated calcinosis cutis identifies potential therapeutic targets and reveals mechanisms resembling those in other calcifying disorders.
Indexed as
Identifiers
What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.