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Cited by 74Renal Transplantation Outcomes and TreatmentsOrgan Transplantation Techniques and OutcomesAcute Kidney Injury Research

Ischemia-reperfusion injury in kidney transplantation: mechanisms and potential therapeutic targets

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Lasorsa, Francesco, Rutigliano, Monica, Milella, Martina, d’Amati, Antonio, Crocetto, Felice, Pandolfo, Savio Domenico, Barone, Biagio, Ferro, Matteo +4 more·2024·International Journal of Molecular Sciences
DOI 10.3390/ijms25084332PMC PMC11050495
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Abstract

Kidney transplantation offers a longer life expectancy and a better quality of life than dialysis to patients with end-stage kidney disease. Ischemia–reperfusion injury (IRI) is thought to be a cornerstone in delayed or reduced graft function and increases the risk of rejection by triggering the immunogenicity of the organ. IRI is an unavoidable event that happens when the blood supply is temporarily reduced and then restored to an organ. IRI is the result of several biological pathways, such as transcriptional reprogramming, apoptosis and necrosis, innate and adaptive immune responses, and endothelial dysfunction. Tubular cells mostly depend on fatty acid (FA) β-oxidation for energy production since more ATP molecules are yielded per substrate molecule than glucose oxidation. Upon ischemia–reperfusion damage, the innate and adaptive immune system activates to achieve tissue clearance and repair. Several cells, cytokines, enzymes, receptors, and ligands are known to take part in these events. The complement cascade might start even before organ procurement in deceased donors. However, additional experimental and clinical data are required to better understand the pathogenic events that take place during this complex process.

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  • Upon reperfusion, abrupt reoxygenation triggers a burst of mitochondrial superoxide production and a transient increase in tissue ROS.

    “Upon reperfusion, abrupt reoxygenation triggers a burst of mitochondrial superoxide production and a transient increase in tissue ROS”

    From Material-dependent oxygen transport governs ischemia-reperfusion injury and drug response in a kidney microphysiological system (2026) · cites this paper as Lasorsa et al., 2024

    Section 2 (Pathophysiology of IRI; page not specified) says restored oxygen supply causes harmful ROS production and that ROS production is higher during reperfusion. Section 3 (Metabolic Reprogramming during IRI; page not specified) identifies mitochondria as a ROS source and superoxide as a mitochondrial ROS. Neither passage establishes a burst specifically of mitochondrial superoxide upon reperfusion or says the tissue ROS increase is transient. (LLM, conf=0.87)

    Experimental — accuracy not yet measured

  • During the ischemic phase, cessation of oxygen and nutrient supply significantly impairs renal metabolism.

    “During the ischemic phase, the cessation of oxygen and nutrient supply significantly impairs renal metabolism”

    From Material-dependent oxygen transport governs ischemia-reperfusion injury and drug response in a kidney microphysiological system (2026) · cites this paper as Lasorsa et al., 2024

    Section 2 (Pathophysiology of IRI; page unavailable) says reduced blood and oxygen supply alter cell metabolism, leading to anaerobic metabolism and lower ATP production. It describes reduced supply rather than complete cessation and does not specifically identify cessation of nutrient supply as a cause. (LLM, conf=0.84)

    Experimental — accuracy not yet measured

  • Rapid reperfusion during the reperfusion phase leads to oxidative stress, mitochondrial dysfunction, and cell death, thereby impairing renal function.

    “rapid reperfusion during the reperfusion phase leads to oxidative stress, mitochondrial dysfunction, and cell death, thereby impairing renal function”

    From Material-dependent oxygen transport governs ischemia-reperfusion injury and drug response in a kidney microphysiological system (2026) · cites this paper as Lasorsa et al., 2024

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Cited by

Sorted by citations

Authors
Lasorsa, F., Rutigliano, M., Milella, M., d’Amati, A., Crocetto, F., Pandolfo, S. D., Barone, B., Ferro, M., Spilotros, M., Battaglia, M., Ditonno, P., & Lucarelli, G.
Affiliations
  • University of Bari Aldo Moro (IT)
  • University of Naples Federico II (IT)
  • University of L'Aquila (IT)
  • Division of Urology, Department of Surgical Sciences, AORN Sant’Anna e San Sebastiano, 81100 Caserta, Italy
  • European Institute of Oncology (IT)
Corresponding author
Lucarelli, Giuseppe
ORCID
Venue
International Journal of Molecular Sciences
Publisher
MDPI AG
Published
2024-04-14
Volume
25
Issue
8
Pages
4332
ISSN
1422-0067 (ISSN-L)
DOI
10.3390/ijms25084332
PMC
PMC11050495
OpenAlex
W4394807907
Cited by
74
References
2
Citations by year
2026: 32 · 2025: 35 · 2024: 7
FWCI
8.44
Type
journal article
Language
en
Open access
Licence
Locations
  • International Journal of Molecular Sciences (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • Archivio Istituzionale della Ricerca (Universita Degli Studi Di Milano) (submittedVersion, other-oa)
  • Archivio Istituzionale della Ricerca - Università degli Studi dell Aquila (submittedVersion, cc-by)
  • CINECA IRIS Institutional Research Information System (University of Bari Aldo Moro) (submittedVersion, cc-by)
Topics
  • Health Sciences › Medicine › Transplantation › Renal Transplantation Outcomes and Treatments
  • Health Sciences › Medicine › Surgery › Organ Transplantation Techniques and Outcomes
  • Health Sciences › Medicine › Nephrology › Acute Kidney Injury Research
Keywords
ischemia-reperfusion injury, kidney transplantation, delayed graft function, graft rejection, end-stage renal disease, fatty acid beta-oxidation, tubular cells, apoptosis, necrosis, innate immune response, adaptive immune response, endothelial dysfunction, complement system, therapeutic target
MeSH terms
Animals, Humans, Reperfusion Injury, Kidney Transplantation

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