Dual Time-Dependent Effects of Interleukin-33 Administration on the Kidney Postmyocardial Infarction.

IF 1.9 4区 医学 Q4 BIOCHEMISTRY & MOLECULAR BIOLOGY Journal of Interferon and Cytokine Research Pub Date : 2024-11-01 Epub Date: 2024-09-23 DOI:10.1089/jir.2024.0127
Ghadir Amin, Rana Ghali, Nada J Habeichi, Ziad Mallat, George W Booz, Fouad A Zouein
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Abstract

Kidney damage is a serious prevalent complication that occurs after a myocardial infarction (MI) and is associated with worse outcomes. Interleukin-33 (IL-33), a member of the IL-1 superfamily, functions as an alarmin that is released upon necrosis or tissue damage to alert immune cells expressing the ST2L receptor. IL-33 is increased in kidney disease, and recent studies have shown that the IL-33/ST2 axis is instrumental in both disease progression and repair. In this study, we investigated the effect of IL-33 administration on kidneys in C57BL6/J male mice 4 and 7 days after the induction of MI. The mice received either IL-33 or vehicle (PBS) treatment. Cardiac systolic function and systemic inflammation were assessed, and kidneys were subjected to histological and molecular analysis. The administration of IL-33 for 4 days post-MI improved renal structure consistent with reduced expression of profibrotic markers, reduced apoptosis, and increased expression of the anti-inflammatory cytokine IL-4. In addition, IL-33 administration enhanced the levels of Sirtuin3, nicotinamide phosphoribosyltransferase, and the renal nicotinamide adenine dinucleotide pool which are critical for mitochondrial function and energy production, indicating metabolic benefits. However, this protection seems to be lost with the continued administration of IL-33 for 7 days post-MI coinciding with aggravated cardiac dysfunction and increased systemic inflammation. These findings demonstrate that while IL-33 treatment can help improve kidney damage post-MI in the short term, extended treatment may not be beneficial. This may be due to the direct effects of IL-33 on the kidneys or indirectly mediated by adverse cardiac remodeling influencing the cardiorenal crosstalk.

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心肌梗死后服用白细胞介素-33对肾脏的双重时间依赖效应
肾脏损伤是心肌梗死(MI)后发生的一种严重并发症,与预后恶化有关。白细胞介素-33(IL-33)是 IL-1 超家族的成员之一,在组织坏死或受损时会释放一种警报素,以提醒表达 ST2L 受体的免疫细胞。IL-33在肾脏疾病中会增加,最近的研究表明,IL-33/ST2轴在疾病进展和修复中都起着重要作用。在本研究中,我们调查了诱导 MI 4 天和 7 天后服用 IL-33 对 C57BL6/J 雄性小鼠肾脏的影响。小鼠接受 IL-33 或载体(PBS)治疗。对心脏收缩功能和全身炎症进行了评估,并对肾脏进行了组织学和分子分析。诱发心肌梗死后 4 天服用 IL-33 可改善肾脏结构,这与损伤性标志物表达减少、细胞凋亡减少和抗炎细胞因子 IL-4 表达增加是一致的。此外,IL-33 还能提高 Sirtuin3、烟酰胺磷酸核糖转移酶和肾脏烟酰胺腺嘌呤二核苷酸池的水平,而这些物质对线粒体功能和能量产生至关重要,这表明IL-33 对新陈代谢有益。然而,在心肌梗死后继续服用 IL-33 7 天后,这种保护作用似乎消失了,同时心脏功能障碍加重,全身炎症加剧。这些研究结果表明,虽然 IL-33 治疗有助于在短期内改善心肌梗死后的肾损伤,但延长治疗时间可能并无益处。这可能是由于 IL-33 对肾脏的直接作用,也可能是由影响心肾串联的不良心脏重塑间接介导的。
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来源期刊
CiteScore
3.80
自引率
0.00%
发文量
78
审稿时长
2.2 months
期刊介绍: Journal of Interferon & Cytokine Research (JICR) provides the latest groundbreaking research on all aspects of IFNs and cytokines. The Journal delivers current findings on emerging topics in this niche community, including the role of IFNs in the therapy of diseases such as multiple sclerosis, the understanding of the third class of IFNs, and the identification and function of IFN-inducible genes.
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