New Insights in Molecular Mechanisms and Pathophysiology of Ischemia-Reperfusion Injury 2.0: An Updated Overview

Panisello‐Roselló, Arnau; Roselló‐Catafau, Joan; Adam, René

doi:10.3390/ijms22010028

Cited by 6 publications

(5 citation statements)

References 36 publications

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“…Ischemia/reperfusion injury is a pathological process caused by tissue ischemia followed by restoration of perfusion, which together initiate a cascade of cellular events culminating in the tissue injury due to the generation of oxidative stress, initiation of the cell death pathways and generation of pro-inflammatory molecules 22 . In the context of trauma-induced hemorrhagic shock, post-trauma resuscitation induces ischemia/reperfusion in tissues and contributes to systemic inflammation and organ dysfunction.…”

Section: Discussionmentioning

confidence: 99%

Effect of remote ischemic conditioning on the immune-inflammatory profile in patients with traumatic hemorrhagic shock in a randomized controlled trial

Leung

Rizoli

Trypcic

et al. 2023

Sci Rep

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Resuscitation induced ischemia/reperfusion predisposes trauma patients to systemic inflammation and organ dysfunction. We investigated the effect of remote ischemic conditioning (RIC), a treatment shown to prevent ischemia/reperfusion injury in experimental models of hemorrhagic shock/resuscitation, on the systemic immune-inflammatory profile in trauma patients in a randomized trial. We conducted a prospective, single-centre, double-blind, randomized, controlled trial involving trauma patients sustaining blunt or penetrating trauma in hemorrhagic shock admitted to a Level 1 trauma centre. Patients were randomized to receive RIC (four cycles of 5-min pressure cuff inflation at 250 mmHg and deflation on the thigh) or a Sham intervention. The primary outcomes were neutrophil oxidative burst activity, cellular adhesion molecule expression, and plasma levels of myeloperoxidase, cytokines and chemokines in peripheral blood samples, drawn at admission (pre-intervention), 1 h, 3 h, and 24 h post-admission. Secondary outcomes included ventilator, ICU and hospital free days, incidence of nosocomial infections, 24 h and 28 day mortality. 50 eligible patients were randomized; of which 21 in the Sham group and 18 in the RIC group were included in the full analysis. No treatment effect was observed between Sham and RIC groups for neutrophil oxidative burst activity, adhesion molecule expression, and plasma levels of myeloperoxidase and cytokines. RIC prevented significant increases in Th2 chemokines TARC/CCL17 (P < 0.01) and MDC/CCL22 (P < 0.05) at 24 h post-intervention in comparison to the Sham group. Secondary clinical outcomes were not different between groups. No adverse events in relation to the RIC intervention were observed. Administration of RIC was safe and did not adversely affect clinical outcomes. While trauma itself modified several immunoregulatory markers, RIC failed to alter expression of the majority of markers. However, RIC may influence Th2 chemokine expression in the post resuscitation period. Further investigation into the immunomodulatory effects of RIC in traumatic injuries and their impact on clinical outcomes is warranted.ClinicalTrials.gov number: NCT02071290.

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Section: Discussionmentioning

confidence: 99%

Effect of remote ischemic conditioning on the immune-inflammatory profile in patients with traumatic hemorrhagic shock in a randomized controlled trial

Leung

Rizoli

Trypcic

et al. 2023

Sci Rep

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“…Recent and growing evidence strongly supports the notion that mitochondria is "where everything happens" that is where ischemia-reperfusion begins within the cell. Research in this topic is still in its infancy, since most data come from animal models and similar clinical conditions, in primis cardiac arrest [12][13][14][15][16][17] . Investigations on uDCDs most often focus on ex-vivo reperfusion (mainly liver) and results are too often difficult to compare due to differences in protocols from one transplant center to another (i.e.…”

Section: Ischemia-reperfusion Phenomenon In the Udcd Donormentioning

confidence: 99%

Uncontrolled Donation After Circulatory Death: A by-Product of the Controlled? A Narrative Review

Lazzeri

Peris

2023

EJT

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“…The reconstruction of blood flow is essential to salvage ischemic tissue. However, it is a double-edged sword, as reperfusion can cause further damage and threaten normal organ function and viability ( 3 , 4 ).…”

Section: Introductionmentioning

confidence: 99%

Gene signature and prediction model of the mitophagy-associated immune microenvironment in renal ischemia-reperfusion injury

Chen

Xie

et al. 2023

Front. Immunol.

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BackgroundRenal ischemia-reperfusion injury (IRI) is an inevitable occurrence during kidney transplantation. Mitophagy, ferroptosis, and the associated immune microenvironment (IME) have been shown to play important roles in renal IRI. However, the role of mitophagy-associated IME genes in IRI remains unclear. In this study, we aimed to construct a prediction model of IRI prognosis based on mitophagy-associated IME genes.MethodThe specific biological characteristics of the mitophagy-associated IME gene signature were comprehensively analyzed using public databases such as GEO, Pathway Unification, and FerrDb. Correlations between the expression of prognostic genes and immune-related genes and IRI prognosis were determined by Cox regression, LASSO analysis, and Pearson’s correlation. Molecular validation was performed using human kidney 2 (HK2) cells and culture supernatant as well as the serum and kidney tissues of mice after renal IRI. Gene expression was measured by PCR, and inflammatory cell infiltration was examined by ELISA and mass cytometry. Renal tissue damage was characterized using renal tissue homogenate and tissue sections.ResultsThe expression of the mitophagy-associated IME gene signature was significantly correlated with IRI prognosis. Excessive mitophagy and extensive immune infiltration were the primary factors affecting IRI. In particular, FUNDC1, SQSTM1, UBB, UBC, KLF2, CDKN1A, and GDF15 were the key influencing factors. In addition, B cells, neutrophils, T cells, and M1 macrophages were the key immune cells present in the IME after IRI. A prediction model for IRI prognosis was constructed based on the key factors associated with the mitophagy IME. Validation experiments in cells and mice indicated that the prediction model was reliable and applicable.ConclusionWe clarified the relationship between the mitophagy-related IME and IRI. The IRI prognostic prediction model based on the mitophagy-associated IME gene signature provides novel insights on the prognosis and treatment of renal IRI.

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New Insights in Molecular Mechanisms and Pathophysiology of Ischemia-Reperfusion Injury 2.0: An Updated Overview

Abstract: Ischemia reperfusion injury (IRI) is related to different surgical interventions such as organ resection and transplantation, and therefore its prevention is of great interest [...]

Cited by 6 publications

References 36 publications

Effect of remote ischemic conditioning on the immune-inflammatory profile in patients with traumatic hemorrhagic shock in a randomized controlled trial

Effect of remote ischemic conditioning on the immune-inflammatory profile in patients with traumatic hemorrhagic shock in a randomized controlled trial

Uncontrolled Donation After Circulatory Death: A by-Product of the Controlled? A Narrative Review

Gene signature and prediction model of the mitophagy-associated immune microenvironment in renal ischemia-reperfusion injury

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