Apelin-13 alleviate inflammatory reaction of ischemia reperfusion in rat kidney transplantation via NF-kappa B signaling pathway

  1. Irene Capelli
  2. Valeria Aiello
  3. Lorenzo Gasperoni
  4. Gaetano La Manna

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Abstract

Backgroud

Kidney transplantation is the optimal treatment for end-stage renal disease, yet acute rejection remains a significant challenge to the survival rates of grafts. Ischemia-reperfusion injury (IRI) can initiate an inflammatory response that severely damages the transplanted kidney.

Methods

The APJ/apelin system has been shown to play an anti-inflammatory role across various domains, and in this study, we utilized apelin-13 in a rat kidney transplantation model to investigate its effects on IRI-related inflammation.

Results

Our findings indicate that apelin predominantly localizes in the renal cortex, and following kidney transplantation, there was destruction of tissue structure and an inflammatory response targeting the transplanted kidney. The administration of apelin-13 led to improved kidney function, reduced organizational structure damage, and lower injury and apoptosis indices compared to the control group. Notably, following the administration of apelin-13, the expression levels of pro-inflammatory cytokines, such as TNF-α, IL-6, and IL-1β, were reduced in comparison to the model control group, as determined by immunofluorescence, western blot, and ELISA Manuscript File Click here to view linked References assays. Furthermore, the extent of CD3 T cell infiltration was lower relative to that in the model control group. We specifically examined the classical inflammation signaling pathway, NF-κB. Our results show that, compared to the model group, the administration of apelin-13 reduced the expression of NF-κB signaling pathway proteins, as evidenced by both immunohistochemistry and western blot analyses.

Conclusions

In conclusion, apelin-13 appears to reduce the inflammatory response to ischemia-reperfusion injury following kidney transplantation, partly through the NF-κB signaling pathway.

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    Review Comments for Manuscript: WITHDRAWN: Apelin-13 alleviate inflammatory reaction of ischemia reperfusion in rat kidney transplantation via NF-kappa B signaling pathway

    (DOI: 10.1101/2024.05.10.593511)

    Recommendation: Do not consider for publication in any form. The preprint has been officially withdrawn and must not be cited or used as scientific reference.

    Summary of the manuscript status:

    This preprint was posted on bioRxiv on May 14, 2024, but was formally withdrawn shortly thereafter (version 2, posted May 23, 2024) following an official request from the Dean of the Department of Medical and Surgical Sciences (DIMEC) at the University of Bologna.

    Reason for withdrawal (official statement from bioRxiv):

    - The submission was fraudulent, carried out by a third party impersonating Prof. Gaetano La Manna (University of Bologna).

    - The corresponding author email was invalid and not the institutional email of Prof. La Manna.

    - The listed authors (Irene Capelli, Valeria Aiello, Lorenzo Gasperoni, and Gaetano La Manna) had no knowledge of or involvement in the work.

    - The department originally cited in the affiliation (DIMES) was dissolved on December 31, 2022, and no longer exists at the time of submission.

    - Note: A real Prof. Gaetano La Manna does exist at the University of Bologna (now in DIMEC, Nephrology), but he is not connected to this manuscript in any way.

    Scientific content (for completeness, though irrelevant due to fraud):

    Because the manuscript was fraudulently submitted and the listed authors disclaim all responsibility, no legitimate scientific evaluation is possible or appropriate. Any data, methods, results, or conclusions presented cannot be attributed to the named researchers and must be considered unreliable and potentially fabricated by the impersonator.

    Additional comments:

    - This incident highlights ongoing issues with third-party fraud and impersonation on preprint servers.

    - Reviewers, editors, and readers are strongly advised to disregard this preprint entirely and remove any citations if they have inadvertently appeared in other works.

    - The DOI remains active for transparency, but the page now displays only the withdrawal notice.

    In summary, this is not a legitimate scientific contribution and should play no role in the peer-review process or the scientific record.

    Competing interests

    The authors declare that they have no competing interests.

    Use of Artificial Intelligence (AI)

    The authors declare that they used generative AI to come up with new ideas for their review.

  2. Version published to 10.1101/2024.05.10.593511 on bioRxiv