ReviewHuman immunology2012
Targeting the intragraft microenvironment and the development of chronic allograft rejection.
Review in Human immunology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
14 citing papers in PubMed, 21 citations in OpenAlex.
- Regulatory T cells in cardiac allograft vasculopathy: from mechanistic insights to clinical tolerance.Frontiers in immunology · 2026Review
- Immunomodulation by allograft endothelial cells.Frontiers in transplantation · 2025Review
- Biomarkers from subcutaneous engineered tissues predict acute rejection of organ allografts.Science advances · 2024Article
- Notch3 expression in capillary pericytes predicts worse graft outcome in human renal grafts with antibody-mediated rejection.Journal of cellular and molecular medicine · 2022Article
- Immunotherapy and Antivascular Targeted Therapy in Patients' Treatment with Concurrent Malignant Tumors after Organ Transplantation: Opportunity or Challenge.Journal of immunology research · 2022Review
- Immune responses to bioengineered organs.Current opinion in organ transplantation · 2017Article
- Article
- Translational implications of endothelial cell dysfunction in association with chronic allograft rejection.Pediatric nephrology (Berlin, Germany) · 2016Review
- Markers of Endothelial-to-Mesenchymal Transition: Evidence for Antibody-Endothelium Interaction during Antibody-Mediated Rejection in Kidney Recipients.Journal of the American Society of Nephrology : JASN · 2016Article
- Regulation of mTOR Signaling by Semaphorin 3F-Neuropilin 2 Interactions In Vitro and In Vivo.Scientific reports · 2015Article
- ABO-compatible liver allograft antibody-mediated rejection: an update.Current opinion in organ transplantation · 2015Review
- Chronic allograft rejection: a fresh look.Current opinion in organ transplantation · 2015Review
- Purinergic signaling in early inflammatory events of the foreign body response: modulating extracellular ATP as an enabling technology for engineered implants and tissues.Tissue engineering. Part B, Reviews · 2014Review
- DEPTOR regulates vascular endothelial cell activation and proinflammatory and angiogenic responses.Blood · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
In this review, we discuss a paradigm whereby changes in the intragraft microenvironment promote or sustain the development of chronic allograft rejection. A key feature of this model involves the microvasculature including (a) endothelial cell (EC) destruction, and (b) EC proliferation, both of which result from alloimmune leukocyte- and/or alloantibody-induced responses. These changes in the microvasculature likely create abnormal blood flow patterns and thus promote local tissue hypoxia. Another feature of the chronic rejection microenvironment involves the overexpression of vascular endothelial growth factor (VEGF). VEGF stimulates EC activation and proliferation and it has potential to sustain inflammation via direct interactions with leukocytes. In this manner, VEGF may promote ongoing tissue injury. Finally, we review how these events can be targeted therapeutically using mTOR inhibitors. EC activation and proliferation as well as VEGF-VEGFR interactions require PI-3K/Akt/mTOR intracellular signaling. Thus, agents that inhibit this signaling pathway within the graft may also target the progression of chronic rejection and thus promote long-term graft survival.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.