ReviewMolecular medicine reports2026
POSTN(+) fibroblasts and SPP1(+) macrophages in scar formation: A review of mechanisms and therapeutic targets (Review).
Review in Molecular medicine reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- Article
Corrections and comments
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Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Scar formation is a physiological process that occurs as a repair mechanism following tissue damage, often presenting as scar tissue at the site of injury. This process entails intricate biological responses that are intended to restore both the structure and function of the damaged tissue. Fibroblasts, the principal cells involved in scar tissue formation, are responsible for synthesizing collagen and various extracellular matrix components, all of which are vital for restoring tissue structure. During the inflammatory phase, macrophages fulfill a critical role through clearing dead cells and pathogens, and also by secreting cytokines that regulate fibroblast activity, thereby promoting the healing process. Recent studies have demonstrated that macrophages labeled with secreted phosphoprotein 1 (SPP1) and fibroblasts labeled with periostin (POSTN) are essential for scar formation, and their interaction may represent a crucial element in this process. Through performing literature searches, the aim of the present study was to further investigate the roles and mechanisms of SPP1(+) macrophages and POSTN(+) fibroblasts in scar formation, highlighting their potential synergistic crosstalk as a novel driver of fibrosis. Furthermore, the present study systematically analyzed their individual contributions, their interaction via signaling pathways and the molecular mechanisms underlying their pro‑fibrotic effects, thereby filling a critical gap in current research by focusing on specific cellular subpopulations. Furthermore, the clinical implications of targeting these specific cell subsets are discussed and this discussion provides valuable insights into the pathophysiology of these conditions, thereby establishing a theoretical basis for the development of targeted therapies for abnormal scar formation.
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Registered trials
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