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Biological pathways and potential targets for prevention and therapy of chronic allograft nephropathy
Badri Man Shrestha1, John Haylor1
1Division of Renal Transplantation, Sheffield Kidney Institute, Northern General Hospital, Herries Road, Sheffield S5 7AU, UK.
Abstract:
Renal transplantation (RT) is the best option for patients with end-stage renal disease, but the half-life is limited to a decade due to progressive deterioration of renal function and transplant failure from chronic allograft nephropathy (CAN), which is the leading cause of transplant loss. Extensive research has been done to understand the pathogenesis, the biological pathways of fibrogenesis, and potential therapeutic targets for the prevention and treatment of CAN. Despite the advancements in the immunosuppressive agents and patient care, CAN continues to remain an unresolved problem in renal transplantation. The aim of this paper is to undertake a comprehensive review of the literature on the pathogenesis, biological pathways of RT fibrogenesis, and potential therapeutic targets for the prevention and therapy of CAN.
Insights
Renal transplantation (RT) offers the best survival for end-stage renal disease but faces limited graft half-life due to chronic allograft nephropathy (CAN). This review explores CAN pathogenesis and therapeutic targets to improve long-term transplant success.
Area of Science:
- Nephrology
- Transplantation Immunology
- Fibrosis Research
Background:
- Renal transplantation (RT) is the optimal treatment for end-stage renal disease, offering superior survival rates.
- Chronic allograft nephropathy (CAN) significantly limits graft half-life, leading to transplant failure and representing the primary cause of graft loss.
- Despite advancements in immunosuppression and patient care, CAN remains a critical unresolved challenge in RT.
Purpose of the Study:
- To conduct a comprehensive literature review on the pathogenesis of CAN.
- To elucidate the biological pathways involved in RT fibrogenesis.
- To identify and discuss potential therapeutic targets for CAN prevention and treatment.
Main Methods:
- Systematic review of existing literature.
- Analysis of studies focusing on fibrogenesis pathways in renal allografts.
- Identification of therapeutic strategies from published research.
Main Results:
- CAN pathogenesis involves complex molecular and cellular mechanisms leading to fibrosis.
- Key fibrotic pathways and mediators have been identified.
- Several potential therapeutic targets for mitigating CAN progression are emerging.
Conclusions:
- Understanding CAN pathogenesis is crucial for developing effective interventions.
- Targeting specific fibrotic pathways holds promise for improving long-term renal allograft survival.
- Further research is needed to translate these findings into clinical practice for CAN management.
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