ArticleMedComm2025
Hypoxia-Driven Neurovascular Impairment Underlies Structural-Functional Dissociation in Diabetic Sudomotor Dysfunction.
Article in MedComm, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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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.
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Who cites it
3 citing papers in PubMed.
- A Multifunctional Nanozyme-Based mRNA Delivery Platform Restores Neurovascular and Sudomotor Function in Diabetic Neuropathy.Advanced healthcare materials · 2026Article
- TLR2-PI3K/Akt mediated microbe-mimetic priming boosts the therapeutic paracrine function of GelMA-Encapsulated MSCs for diabetic wound regeneration.Bioactive materials · 2026Article
- Single-cell mapping of diabetic foot ulcers: mechanistic axes and therapeutic targets.Frontiers in medicine · 2026Review
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Authors and funding
21 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sudomotor dysfunction in diabetic patients increases the risk of fissures, infections, and diabetic foot ulcers (DFUs), thereby reducing the quality of life. Despite its clinical importance, the mechanisms underlying this dysfunction remain inadequately elucidated. This study addresses this gap by demonstrating that despite structural integrity, sweat glands (SGs) in diabetic individuals with DFUs, and a murine model of diabetic neuropathy (DN), exhibit functional impairments, as confirmed by histological and functional assays. Integrated transcriptome and proteome analysis revealed significant upregulation of the SG microenvironment in response to hypoxia, highlighting potential underlying pathways involved. In addition, histological staining and tissue clearing techniques provided evidence of impaired neurovascular networks adjacent to SGs. Single-cell RNA sequencing unveiled intricate intercellular communication networks among endothelial cells (ECs), neural cells (NCs), and sweat gland cells (SGCs), emphasizing intricate cellular interactions within the SG microenvironment. Furthermore, an in vitro SGC-NC interaction model (SNIM) was employed to validate the supportive role of NCs in regulating SGC functions, highlighting the neurovascular-SG axis in diabetic pathophysiology. These findings confirm the hypoxia-driven upregulation of the SG microenvironment and underscore the critical role of the neurovascular-SG axis in diabetic pathophysiology, providing insights into potential therapeutic targets for managing diabetic complications and improving patient outcomes.
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Registered trials
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