{
  "abstract": "Background\n\nHeart failure with preserved ejection fraction (HFpEF) accounts for half of all heart failure cases. However, its complex pathophysiology, which is characterized by bidirectional interactions among immune, metabolic, and mechanical pathways, has long resisted a simple explanation.Approach\n\nRather than listing parallel mechanisms, this review organizes recent breakthroughs around three cross-cutting frontiers: neuroimmune regulation, cell-type-specific metabolic reprogramming, and mechanotransduction. It then integrates these frontiers within the adipokine hypothesis.Key findings\n\nCardiac macrophage subset imbalance, myeloid fatty acid-driven inflammation, matrix stiffness-mediated feedforward loops, and adipokine imbalance have emerged as interconnected drivers of HFpEF.Conclusion\n\nWith the aid of multi-omics and machine learning, mapping these mechanistic dialogues onto phenotype-targeted precision therapy provides a roadmap for transforming HFpEF from a syndrome defined by ejection fraction into molecularly tractable endotypes.",
  "abstract_shown": true,
  "affiliations": [
    "Department of Cardiology, Ma'anshan People's Hospital, Wannan Medical University, Anhui Ma'anshan, 243099, China.",
    "Graduate School, Wannan Medical University, Anhui Wuhu, 241002, China.",
    "Department of Cardiology, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Anhui Hefei, 230001, China."
  ],
  "article_type": "research support, non u.s. gov't",
  "arxiv": null,
  "author_total": 4,
  "authors": [
    {
      "affs": [
        0
      ],
      "name": "KaiJian Zhang"
    },
    {
      "affs": [
        1,
        2
      ],
      "name": "Hui Li"
    },
    {
      "affs": [
        2
      ],
      "name": "Wei Wen"
    },
    {
      "affs": [
        2
      ],
      "name": "BuChun Zhang"
    }
  ],
  "bibtex": "https://research.draconitic.com/paper/9y4ph2dhbqsdz.bib",
  "cited_by": 0,
  "doi": "10.7150/ijbs.137328",
  "fulltext_url": "https://europepmc.org/articles/PMC13685608",
  "id": "9y4ph2dhbqsdz",
  "issns": [
    "1449-2288"
  ],
  "landing_url": "https://europepmc.org/article/MED/42910211",
  "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": [
    [
      "openalex",
      "2705|Cardiac Fibrosis and Remodeling"
    ]
  ],
  "openalex": "W7214589521",
  "pdf_url": "https://europepmc.org/articles/PMC13685608?pdf=render",
  "pmcid": "PMC13685608",
  "pmid": "42910211",
  "published": "2026-09-11",
  "publisher": null,
  "ris": "https://research.draconitic.com/paper/9y4ph2dhbqsdz.ris",
  "sources": [
    {
      "first_seen": "2026-10-30T12:20:14Z",
      "native_id": "MED:42910211",
      "source": "europepmc",
      "url": "https://europepmc.org/article/MED/42910211"
    }
  ],
  "subjects": [
    {
      "field": "medicine",
      "origin": "openalex:2705|Cardiac Fibrosis and Remodeling",
      "subfield": "cardiovascular"
    }
  ],
  "title": "Cross-cutting circuits in heart failure with preserved ejection fraction: Integrating adipokine biology, mechanotransduction, and precision targeting.",
  "title_text": "Cross-cutting circuits in heart failure with preserved ejection fraction: Integrating adipokine biology, mechanotransduction, and precision targeting.",
  "type": "peer-reviewed",
  "updated_at": "2026-10-30T12:20:14Z",
  "url": "https://research.draconitic.com/paper/9y4ph2dhbqsdz",
  "venue": "International journal of biological sciences",
  "versions": []
}