{
  "abstract": "Background: Alzheimer’s disease (AD) is characterized by amyloid-β accumulation, mitochondrial dysfunction, and neuronal injury. miR-615-3p is upregulated in AD, but its role in regulating mitophagy remains unclear.\n\nMethods: HT22 hippocampal neurons were treated with Aβ1-42 to establish an AD-like model. Gain-of-function and loss-of-function experiments were conducted to assess the roles of miR-615-3p and its target SESN2, which were identified through bioinformatics and dual-luciferase assays. Cell viability, apoptosis, oxidative stress, mitochondrial function, inflammatory responses, and mitophagy-related proteins were evaluated. The involvement of the AMPK/ULK1 pathway was also examined.\n\nResults: miR-615-3p overexpression significantly reduced cell viability and ATP levels while increasing apoptosis, Aβ accumulation, lactate dehydrogenase release, reactive oxygen species production, mitochondrial membrane potential loss, and inflammatory cytokine levels. Mitophagy markers, including LC3-II/LC3-I, Parkin, and PINK1, were elevated. Mechanistically, miR-615-3p downregulated SESN2 and inhibited AMPK/ULK1 phosphorylation. SESN2 overexpression reversed these effects, restoring mitochondrial function, reducing oxidative stress and inflammation, and improving cell survival.\n\nConclusion: miR-615-3p aggravates neuronal injury by targeting SESN2 and regulating mitophagy through the AMPK/ULK1 pathway, suggesting a potential therapeutic target for Alzheimer’s disease.",
  "abstract_shown": true,
  "affiliations": [
    "Department of Xiaolong Internal Medicine, Nanchong Psychosomatic Hospital , ,"
  ],
  "article_type": "research article",
  "arxiv": null,
  "author_total": 5,
  "authors": [
    {
      "affs": [
        0
      ],
      "name": "Yang Jing"
    },
    {
      "affs": [
        0
      ],
      "name": "DeKun Li"
    },
    {
      "affs": [
        0
      ],
      "name": "Li Chen"
    },
    {
      "affs": [
        0
      ],
      "name": "Song Li"
    },
    {
      "affs": [
        0
      ],
      "name": "Xiang Yuan"
    }
  ],
  "bibtex": "https://research.draconitic.com/paper/b7kq8kfvhhd2x.bib",
  "cited_by": 0,
  "doi": "10.3389/fnmol.2026.1873619",
  "fulltext_url": "https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13719307/?tool=EBI",
  "id": "b7kq8kfvhhd2x",
  "issns": [
    "1662-5099"
  ],
  "landing_url": "https://europepmc.org/article/PMC/PMC13719307",
  "language": "eng",
  "licence": "CC-BY",
  "licence_label": "CC BY",
  "licence_source": "article",
  "licence_url": "https://creativecommons.org/licenses/by/4.0/",
  "metadata_licence": null,
  "native_subjects": [
    [
      "heading",
      "Original Research"
    ],
    [
      "openalex",
      "2737|Alzheimer's disease research and treatments"
    ]
  ],
  "openalex": "W7222633110",
  "pdf_url": "https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13719307/pdf/?tool=EBI",
  "pmcid": "PMC13719307",
  "pmid": "42964017",
  "published": "2026-10-16",
  "publisher": "Frontiers Media SA",
  "ris": "https://research.draconitic.com/paper/b7kq8kfvhhd2x.ris",
  "sources": [
    {
      "first_seen": "2026-10-31T12:21:36Z",
      "native_id": "PMC:PMC13719307",
      "source": "europepmc",
      "url": "https://europepmc.org/article/PMC/PMC13719307"
    },
    {
      "first_seen": "2026-11-02T12:23:17Z",
      "native_id": "PMC13719307",
      "source": "pmc",
      "url": "https://doi.org/10.3389/fnmol.2026.1873619"
    }
  ],
  "subjects": [
    {
      "field": "medicine",
      "origin": "openalex:2737|Alzheimer's disease research and treatments",
      "subfield": "physiology"
    }
  ],
  "title": "miR-615-3p targets SESN2 to inhibit neuronal mitophagy in an in vitro Alzheimer’s disease model by regulating the AMPK/ULK1 axis",
  "title_text": "miR-615-3p targets SESN2 to inhibit neuronal mitophagy in an in vitro Alzheimer’s disease model by regulating the AMPK/ULK1 axis",
  "type": "peer-reviewed",
  "updated_at": "2026-11-03T12:20:23Z",
  "url": "https://research.draconitic.com/paper/b7kq8kfvhhd2x",
  "venue": "Frontiers in molecular neuroscience",
  "versions": []
}