Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Pro‐inflammatory immunity supports fibrosis advancement in epidermolysis bullosa: intervention with Ang‐(1‐7)

30 Aug 2021

Abstract excerpt

Recessive dystrophic epidermolysis bullosa (RDEB), a genetic skin blistering disease, is a paradigmatic condition of tissue fragility-driven multi-organ fibrosis. Here, longitudinal analyses of the tissue proteome through the course of naturally developing disease in RDEB mice revealed that increased pro-inflammatory immunity associates with fibrosis evolution. Mechanistically, this fibrosis is a consequence of...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Autoimmune Bullous Skin Diseases
Share to Cell Adhesion Molecules Research
Share to Skin and Cellular Biology Research

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 34459121
DOI: 10.15252/emmm.202114392

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 4 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Pro‐inflammatory immunity supports fibrosis advancement in epidermolysis bullosa: intervention with Ang‐(1‐7)PMID 34459121Read ↗

Genomics of Human Fibrotic Diseases: Disordered Wound Healing ResponseSemantic proximity Read ↗

Injury- and inflammation-driven skin fibrosis: The paradigm of epidermolysis bullosaSemantic proximity Read ↗

Diversity of Mechanisms Underlying Latent TGF-β Activation in Recessive Dystrophic Epidermolysis Bullosa.Semantic proximity Read ↗

Shared and distinct mechanisms of fibrosis.Semantic proximity Read ↗

Therapies for genetic extracellular matrix diseases of the skin.Semantic proximity Read ↗

Endotrophin, a Key Marker and Driver for Fibroinflammatory DiseaseSemantic proximity Read ↗

Impaired Wound Healing, Fibrosis, and Cancer: The Paradigm of Recessive Dystrophic Epidermolysis Bullosa.Semantic proximity Read ↗

ADAMTS12 promotes fibrosis by restructuring extracellular matrix to enable activation of injury-responsive fibroblastsSemantic proximity Read ↗

Mechanistic interrogation of mutation-independent disease modulators of RDEB identifies the small leucine-rich proteoglycan PRELP as a TGF-β antagonist and inhibitor of fibrosis.Semantic proximity Read ↗

Monozygotic twins discordant for recessive dystrophic epidermolysis bullosa phenotype highlight the role of TGF-β signalling in modifying disease severity.Semantic proximity Read ↗

Dynamic pathological analysis reveals a protective role against skin fibrosis for TREM2-dependent macrophagesSemantic proximity Read ↗

Fibrosis: ultimate and proximate causes.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.