ArticleJournal of cellular and molecular medicine2021
Bortezomib alleviates antibody-mediated rejection in kidney transplantation by facilitating Atg5 expression.
Article in Journal of cellular and molecular medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.
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Who cites it
9 citing papers in PubMed, 1 synthesis or guideline pooled it, 13 citations in OpenAlex.
- Network meta-analysis of pharmacological treatment for antibody-mediated rejection after organ transplantation.Frontiers in immunology · 2024Pooled it
- Targeting lipophagy in atherosclerosis: Molecular mechanisms, pathogenesis and therapeutic interventions (Review).Molecular medicine reports · 2026Review
- Advances in antibody-mediated rejection of renal allografts.Frontiers in immunology · 2026Review
- What happens to regulatory T cells in multiple myeloma.Cell death discovery · 2023Review
- A bibliometric and knowledge-map analysis of antibody-mediated rejection in kidney transplantation.Renal failure · 2023Article
- The immunomodulation role of Th17 and Treg in renal transplantation.Frontiers in immunology · 2023Review
- The multifunctional roles of autophagy in the innate immune response: Implications for regulation of transplantation rejection.Frontiers in cell and developmental biology · 2022Review
- Bortezomib alleviates antibody-mediated rejection in kidney transplantation by facilitating Atg5 expression.Journal of cellular and molecular medicine · 2021Article
- Antibody-mediated rejection in xenotransplantation: Can it be prevented or reversed?XenotransplantationReview
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Antibody-mediated rejection (AMR) is one of the most dominant mechanisms responsible for the loss of kidney grafts. Previous researches have shown that donor-specific antibodies (DSAs) are the major mediators of AMR. In order to prolong the survival time of grafts, it is vital to reduce the incidence of AMR and inhibit the generation of DSAs. We established an animal model of AMR by performing kidney transplantation in pre-sensitized rats. Then, we investigated the effect of bortezomib (BTZ) on AMR. We found that BTZ could reduce the serum level of DSAs and alleviate post-transplantation inflammation in peritubular capillaries (PTCs) and glomeruli, which was demonstrated by the reduction of C4d and IgG deposition in PTCs, and the reduced number of B cell and plasma cell in peripheral blood and the transplanted kidney (p < 0.05). Our results also suggested that BTZ increased the number of regulatory T cell (Treg) and significantly reduced the proportion of T helper (Th17) cell (p < 0.05). Besides, BTZ induced the significant upregulation of anti-inflammatory cytokines but downregulated pro-inflammatory cytokines (p < 0.05). After dealing with Atg5 siRNA-lentivirus, the effect of BTZ alleviating AMR was reversed and Th17/Treg proportions were also significantly modulated. Collectively, these findings show that BTZ slows down the process of AMR and Atg5 may be the key mechanism. Furthermore, Atg5 silencing results may be demonstrated that Atg5 alleviated AMR by modulating the ratio of Th17/Treg.
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