What is the central question of this study? Renal ischaemia-reperfusion injury occurs in various clinical settings. The clinical diagnosis of ischaemia-reperfusion injury is routinely based on biochemical and haematological tests, which cannot evaluate the function of a single kidney. New magnetic resonance imaging techniques to identify the pathophysiological changes in the renal outer medulla were evaluated. What is the main finding and its importance? This study demonstrated that susceptibility-weighted imaging is a feasible non-invasive tool for imaging and evaluating physipathological changes in the renal outer medulla after ischaemia-reperfusion injury. The aim was to evaluate the feasibility of susceptibility-weighted imaging (SWI) as a tool to identify the changes in the renal outer medulla (OM) in a rabbit model of renal ischaemia-reperfusion injury (IRI). New Zealand rabbits were used (control group n = 10; IRI group n = 40). The rabbits in the IRI group were subjected to left renal artery clamping for 60 min. T2-weighted (T2WI) and SWI examinations were performed at 1, 12, 24 or 48 h after reperfusion (each n = 10). After the examinations, the kidneys were submitted to histological evaluation. The contrast-to-noise ratio (CNR) for the left renal OM was measured using T2WI and SWI. The T2WI and SWI scores of the integrity of the renal OM were evaluated. There were significant differences between T2WI CNRs and SWI CNRs in the control group and the IRI 1, 12 and 48 h time points (all P < 0.05). No significant difference was found between T2WI and SWI CNRs at IRI 24 h (P > 0.05). The mean SWI scores of renal OM in the IRI 1 and 12 h subgroups were both significantly lower than that in the control group (all P < 0.05). The only significant difference in the mean T2WI scores of renal OM was observed between the control and IRI 1 h groups (P < 0.05). Susceptibility-weighted imaging has a significant advantage in evaluation of healthy renal OM over conventional magnetic resonance imaging, and it is a feasible non-invasive tool for imaging and evaluating changes in the renal OM after IRI.
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http://dx.doi.org/10.1113/EP086203 | DOI Listing |
Medicine (Baltimore)
January 2025
Nerve Rehabilitation Center, Beijing Rehabilitation Hospital Affiliated to Capital Medical University, Xixia Zhuang, Badachu, Shijingshan District, Beijing, China.
Ischemic stroke is caused by blockage of blood vessels in brain, affecting normal function. The roles of Signal Transformer and Activator of Transcription 1 (STAT1), CASP8, and MYD88 in ischemic stroke and its care are unclear. The ischemic stroke datasets GSE16561 and GSE180470 were found from the Gene Expression Omnibus database.
View Article and Find Full Text PDFFEBS J
January 2025
INSERM UMR-1100, "Research Center for Respiratory Diseases (CEPR)", Tours, France.
Transplanted organs are inevitably exposed to ischemia-reperfusion (IR) injury, which is known to cause graft dysfunction. Functional and structural changes that follow IR tissue injury are mediated by neutrophils through the production of oxygen-derived free radicals, as well as from degranulation which entails the release of proteases and other pro-inflammatory mediators. Neutrophil serine proteases (NSPs) are believed to be the principal triggers of post-ischemic reperfusion damage.
View Article and Find Full Text PDFFASEB J
January 2025
Department of Hepatobiliary and Pancreatic Surgery, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Liver ischemia-reperfusion (IR) injury is a common complication following liver surgery, significantly impacting the prognosis of liver transplantation and other liver surgeries. Betaine-homocysteine methyltransferase (BHMT), a crucial enzyme in the methionine cycle, has been previously confirmed the pivotal role in hepatocellular carcinoma, and it has also been demonstrated that BHMT inhibits inflammation, apoptosis, but its role in liver IR injury remains unknow. Following I/R injury, we found that BHMT expression was significantly upregulated in human liver transplant specimens, mice and hepatocytes.
View Article and Find Full Text PDFAdv Sci (Weinh)
January 2025
Liver Transplant Center, Transplant Center, West China Hospital, Sichuan University, Chengdu, 610041, China.
Recipients often suffer from hyperlactatemia during liver transplantation (LT), but whether hyperlactatemia exacerbates hepatic ischemia-reperfusion injury (IRI) after donor liver implantation remains unclear. Here, the role of hyperlactatemia in hepatic IRI is explored. In this work, hyperlactatemia is found to exacerbate ferroptosis during hepatic IRI.
View Article and Find Full Text PDFImmun Inflamm Dis
January 2025
Division of Physiology, Department of Molecular Medicine, Institute of Basic Medical Sciences, University of Oslo, Oslo, Norway.
Background: Sepsis is associated with myocardial injury and early mortality. The innate immune receptor Toll-like receptor 4 (TLR4) can recognize pathogen-associated-molecular-patterns (PAMPs) and damage-associated molecular patterns (DAMPs); the latter are released during tissue injury. We hypothesized that TLR4 inhibition reduces proinflammatory signaling and cytokine release in: (1) LPS or Escherichia coli-treated isolated mouse heart; (2) LPS-treated mouse primary adult cardiomyocytes; and (3) the isolated heart during ischemia-reperfusion.
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