Allograft fibrosis represents a key contributor to chronic graft dysfunction and late transplant failure. It arises from continuous tissue injury and dysregulated repair processes associated with immune rejection, resulting in excessive extracellular matrix accumulation. Persistent immune activation, ischemia-reperfusion injury, and drug-induced toxicity stimulate profibrotic signalling pathways, which activate fibroblasts and promote their differentiation into myofibroblasts. These cells drive collagen accumulation and structural distortion within the graft. Recent studies using transcriptomic and proteomic analyses have revealed distinct cellular and molecular mechanisms involved in fibrosis progression, including epithelial-to-mesenchymal transition and immune–stromal interactions. Understanding these pathways provides a foundation for identifying novel therapeutic targets to prevent or reverse fibrosis. Targeted modulation of key signalling cascades may improve long-term graft function and survival, representing a crucial direction for future post-transplant research.

The goal of this research is to elucidate the molecular and cellular mechanisms driving allograft fibrosis and to identify potential therapeutic targets to prevent or reverse this process. Despite advances in immunosuppressive therapy that have improved short-term transplant outcomes, chronic fibrosis remains a leading cause of late graft loss. The problem lies in the incomplete understanding of how persistent immune activation and profibrotic signalling converge to promote fibroblast activation, myofibroblast differentiation, and extracellular matrix accumulation. To address this, the study will integrate recent advances in single-cell transcriptomics, spatial omics, and proteomics to dissect the cellular heterogeneity and intercellular communication within fibrotic grafts. By mapping key signalling pathways, this research aims to identify novel molecular targets for antifibrotic intervention and identifying the source of recipient or donor derived allo-fibroblasts. Ultimately, these insights may guide the development of targeted therapies to improve long-term graft survival and transplant outcomes.

We welcome manuscripts focusing on, but not limited to, the following sub-topics:

• Mechanistic insights into immune-mediated injury and chronic inflammation in allograft fibrosis

• Cellular and molecular pathways driving fibroblast activation and myofibroblast differentiation

• Roles of epithelial-to-mesenchymal and endothelial-to-mesenchymal transitions in graft fibrosis

• Crosstalk between immune cells, stromal cells, and vascular components in fibrotic remodeling.

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Mechanistic insights and therapeutic target discovery in allograft fibrosis post-transplantation