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Purpose of Review <p>Chronic Rejection (CR) has emerged as a major barrier to long-term success in vascularized composite allotransplantation (VCA), yet a unified definition, mechanistic framework and standardized diagnostic criteria remain lacking. This review synthesizes current evidence to clarify how CR manifests across different tissue compartments, identify emerging mechanistic pathways, and outline evolving strategies for detection and monitoring.</p> Recent Findings <p>Clinical and preclinical studies demonstrate that CR in VCA encompasses vascular, fibrotic, and sclerotic patterns arising from recurrent low-grade immune activation, endothelial and stromal injury, and dysregulated tissue repair. Common mechanisms include persistent T-cell-mediated inflammation, progressive vascular remodeling, and pro-fibrotic signaling such as TGF-β-driven matrix deposition. Although donor-specific antibodies and C4d may contribute in select cases, their role remains inconsistent across recipients. Advances in multimodal surveillance – including angiographic imaging, ultrasound biomicroscopy, and elastography – are improving early recognition of chronic changes.</p> Summary <p>CR in VCA represents a multifaceted process rather than a singular endpoint, necessitating integrated clinical, histologic, and imaging approaches. Integrating mechanistic insights with standardized, longitudinal monitoring will be essential to refine diagnostic criteria, detect early injury, and guide strategies to preserve durable graft function.</p>

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“Redefining Chronic Rejection in VCA: A Phenotype-Based Framework for Mechanisms, Diagnosis, and Future Directions”

  • 期刊论文

  • 发表日期：

    2026年2月10日

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  • Anandhini D. Narayanan,
  • Sergio A. Segrera,
  • Alexis K. Gursky,
  • Hailey P. Wyatt,
  • Bruce E. Gelb,
  • Daniel J. Ceradini,
  • Eduardo D. Rodriguez

摘要

Purpose of Review

Chronic Rejection (CR) has emerged as a major barrier to long-term success in vascularized composite allotransplantation (VCA), yet a unified definition, mechanistic framework and standardized diagnostic criteria remain lacking. This review synthesizes current evidence to clarify how CR manifests across different tissue compartments, identify emerging mechanistic pathways, and outline evolving strategies for detection and monitoring.

Recent Findings

Clinical and preclinical studies demonstrate that CR in VCA encompasses vascular, fibrotic, and sclerotic patterns arising from recurrent low-grade immune activation, endothelial and stromal injury, and dysregulated tissue repair. Common mechanisms include persistent T-cell-mediated inflammation, progressive vascular remodeling, and pro-fibrotic signaling such as TGF-β-driven matrix deposition. Although donor-specific antibodies and C4d may contribute in select cases, their role remains inconsistent across recipients. Advances in multimodal surveillance – including angiographic imaging, ultrasound biomicroscopy, and elastography – are improving early recognition of chronic changes.

Summary

CR in VCA represents a multifaceted process rather than a singular endpoint, necessitating integrated clinical, histologic, and imaging approaches. Integrating mechanistic insights with standardized, longitudinal monitoring will be essential to refine diagnostic criteria, detect early injury, and guide strategies to preserve durable graft function.