ArticleProtein & cell2026
Fibulin-7 in progenitor cells promotes adipose tissue fibrosis and disrupts metabolic homeostasis in obesity.
Article in Protein & cell, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- ITIH5 drives adipocyte differentiation and obesity-associated metabolic dysregulation via PI3K/AKT signaling activation.Journal of molecular cell biology · 2026Article
- Helminth infection induces RELMα-dependent adipose tissue transcriptional reprogramming and protection against diet-induced obesity.bioRxiv : the preprint server for biology · 2026Article
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Authors and funding
17 authors.
Funding
Abstract
Fibrosis, resulting from excess extracellular matrix (ECM) deposition, is a feature of adipose tissue (AT) dysfunction and obesity-related insulin resistance. Emerging evidence indicates that adipogenic stem and precursor cells (ASPCs) are a crucial origin of ECM proteins and possess the potential to induce AT fibrosis. Here, we employed single-cell RNA-seq and identified a unique subset of ASPCs that were closely associated with ECM function. Within this subset, we discerned a notable upregulation in the expression of fibulin-7 (FBLN7), a secreted glycoprotein, in obese mice. Similarly, in humans, FBLN7 levels exhibited an increase in visceral fat among obese individuals and demonstrated a correlation with clinical metabolic traits. Functional studies further revealed that, in response to caloric excess, ASPC-specific FBLN7 knockout mice displayed a diminished state of AT fibrosis inflammation, along with improved systemic metabolic health. Notably, the depletion of FBLN7 in ASPCs suppressed TGF-β-induced fibrogenic responses, whereas its overexpression amplified such responses. Mechanistically, FBLN7 interacted with thrombospondin-1 (TSP1) via its EGF-like calcium-binding domain, thereby enhancing the stability of the TSP1 protein. This, in turn, facilitated the conversion of latent TGF-β to its bioactive form, subsequently promoting TGFBR1/Smad signaling pathways. Furthermore, we developed an anti-FBLN7 neutralizing antibody, which could dramatically alleviate diet-induced AT fibrosis. These results suggest that FBLN7, produced by ASPCs, exerts a major influence in the development of AT fibrosis and may represent a potential target for therapeutic intervention.
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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 OpenQuestion graph.