ArticleThe Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation2021
Bone marrow-derived AXL tyrosine kinase promotes mitogenic crosstalk and cardiac allograft vasculopathy.
Article in The Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 10 citations in OpenAlex.
- A modified mouse heart transplant model with extended aorta enables analysis of vascular continuity in cardiac allograft vasculopathy.JHLT open · 2026Article
- Single-cell and spatial transcriptomics identify immune-stromal interactions in cardiac allograft vasculopathy.Nature cardiovascular research · 2026Article
- Suppression of cardiac allograft vasculopathy by a macrophage efferocytosis receptor.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2026Article
- Regulatory T cells in cardiac allograft vasculopathy: from mechanistic insights to clinical tolerance.Frontiers in immunology · 2026Review
- Treg activation during allograft tolerance induction requires mitochondrion-induced TGF-β1 in type 1 conventional dendritic cells.The Journal of clinical investigation · 2025Article
- Best practices of heart transplantation in mice.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2025Review
- Decoding immune cell interactions during cardiac allograft vasculopathy: insights derived from bioinformatic strategies.Frontiers in cardiovascular medicine · 2025Review
- Hypoxia inducible factor 2α promotes tolerogenic macrophage development during cardiac transplantation through transcriptional regulation of colony stimulating factor 1 receptor.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- AXL inhibition suppresses early allograft monocyte-to-macrophage differentiation and prolongs allograft survival.JCI insight · 2024Article
- Alloantigen Infusion Activates the Transcriptome of Type 2 Conventional Dendritic Cells.ImmunoHorizons · 2023Article
- Prognostic Value of Soluble AXL in Serum from Heart Failure Patients with Preserved and Reduced Left Ventricular Ejection Fraction.Journal of personalized medicine · 2023Article
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Authors and funding
15 authors at 4 institutions in 1 country.
Funding
Abstract
Cardiac Allograft Vasculopathy (CAV) is a leading contributor to late transplant rejection. Although implicated, the mechanisms by which bone marrow-derived cells promote CAV remain unclear. Emerging evidence implicates the cell surface receptor tyrosine kinase AXL to be elevated in rejecting human allografts. AXL protein is found on multiple cell types, including bone marrow-derived myeloid cells. The causal role of AXL from this compartment and during transplant is largely unknown. This is important because AXL is a key regulator of myeloid inflammation. Utilizing experimental chimeras deficient in the bone marrow-derived Axl gene, we report that Axl antagonizes cardiac allograft survival and promotes CAV. Flow cytometric and histologic analyses of Axl-deficient transplant recipients revealed reductions in both allograft immune cell accumulation and vascular intimal thickness. Co-culture experiments designed to identify cell-intrinsic functions of Axl uncovered complementary cell-proliferative pathways by which Axl promotes CAV-associated inflammation. Specifically, Axl-deficient myeloid cells were less efficient at increasing the replication of both antigen-specific T cells and vascular smooth muscle cells (VSMCs), the latter a key hallmark of CAV. For the latter, we discovered that Axl-was required to amass the VSMC mitogen Platelet-Derived Growth Factor. Taken together, our studies reveal a new role for myeloid Axl in the progression of CAV and mitogenic crosstalk. Inhibition of AXL-protein, in combination with current standards of care, is a candidate strategy to prolong cardiac allograft survival.
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