{
  "abstract": "Background: Sepsis-associated acute kidney injury (S-AKI) is frequently accompanied by albuminuria, highlighting the need to protect the glomerular filtration barrier during systemic inflammation. The cholinergic anti-inflammatory pathway (CAP) limits inflammatory responses through α7 nicotinic acetylcholine receptors (α7nAChR), but CAP-based renoprotection has been mainly studied in immune and tubular compartments. Here we tested whether α7nAChR activation directly protects podocytes in S-AKI.\n\nResults: In an LPS-induced mouse model, pretreatment with the α7nAChR agonist GTS-21 improved renal function, reduced albuminuria, preserved podocyte ultrastructure, and maintained nephrin, podocin, synaptopodin, and podocalyxin; it also partially restored ZO-1 organization in glomerular and tubular compartments. Chrna7 signals were broadly distributed within glomeruli, with partial colocalization with the podocyte marker podocin; α7nAChR expression was also detected in cultured podocytes. Using podocyte-specific Chrna7 knockout mice, we show that podocyte Chrna7 deletion attenuated GTS-21–mediated reductions in albuminuria and blunted preservation of podocyte markers and glomerular ZO-1, indicating that podocyte α7nAChR substantially contributes to the glomerular protective effects of α7nAChR activation. In cultured podocytes, GTS-21 preserved synaptopodin and improved ZO-1 continuity under LPS challenge. Transcriptomic analysis and time-course studies revealed that α7nAChR activation blunted LPS-induced NF-κB signaling, including p65 nuclear translocation, phosphorylation, and target gene expression.\n\nConclusions: Together, these findings identify podocytes as a direct CAP/α7 target and support α7 activation as a multi-compartment strategy to preserve glomerular barrier integrity in septic kidney injury.",
  "abstract_shown": true,
  "affiliations": [],
  "article_type": null,
  "arxiv": null,
  "author_total": 8,
  "authors": [
    {
      "name": "Aobing Yang"
    },
    {
      "name": "Chia-Hsien Wu",
      "orcid": "0000-0002-2487-2984"
    },
    {
      "name": "Kotaro Shimoyama"
    },
    {
      "name": "Ryoko Yamamoto"
    },
    {
      "name": "Ryusuke Umene"
    },
    {
      "name": "Yasuna Nakamura"
    },
    {
      "name": "Yuan Zhang"
    },
    {
      "name": "Tsuyoshi Inoue"
    }
  ],
  "bibtex": "https://research.draconitic.com/paper/7wwph1zja8prz.bib",
  "cited_by": 0,
  "doi": "10.1186/s12915-026-02758-6",
  "fulltext_url": null,
  "id": "7wwph1zja8prz",
  "issns": [
    "1741-7007"
  ],
  "landing_url": "https://link.springer.com/10.1186/s12915-026-02758-6",
  "language": null,
  "licence": "CC-BY-4.0",
  "licence_label": "CC BY 4.0",
  "licence_source": "article",
  "licence_url": "https://creativecommons.org/licenses/by/4.0",
  "metadata_licence": null,
  "native_subjects": [
    [
      "openalex",
      "2727|Renal Diseases and Glomerulopathies"
    ]
  ],
  "openalex": "W7220990455",
  "pdf_url": null,
  "pmcid": null,
  "pmid": null,
  "published": "2026-10-08",
  "publisher": "Springer Science and Business Media LLC",
  "ris": "https://research.draconitic.com/paper/7wwph1zja8prz.ris",
  "sources": [
    {
      "first_seen": "2026-10-30T12:19:05Z",
      "native_id": "10.1186/s12915-026-02758-6",
      "source": "crossref",
      "url": "https://link.springer.com/10.1186/s12915-026-02758-6"
    }
  ],
  "subjects": [
    {
      "field": "biochemistry",
      "origin": "journal-openalex:1312|Genomics and Phylogenetic Studies",
      "subfield": "molecular-biology"
    },
    {
      "field": "biology",
      "origin": "issn:1741-7007",
      "subfield": "general"
    }
  ],
  "title": "Alpha-7 nicotinic acetylcholine receptor activation preserves podocyte integrity during sepsis-associated kidney injury",
  "title_text": "Alpha-7 nicotinic acetylcholine receptor activation preserves podocyte integrity during sepsis-associated kidney injury",
  "type": "peer-reviewed",
  "updated_at": "2026-10-30T12:19:05Z",
  "url": "https://research.draconitic.com/paper/7wwph1zja8prz",
  "venue": "BMC Biology",
  "versions": []
}