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Home About Traditions &＃038; History Careers at YCU Academics Undergraduate Study School of International Liberal Arts School of Economics and Business Administration School of Science School of Data Science School of Medicine School of Medicine: Medical Course School of Medicine: Nursing Course Graduate Study Graduate School of Urban Social and Cultural Studies Graduate School of International Management Graduate School of Nanobioscience Graduate School of Nanobioscience: Department of Materials System Science Graduate School of Nanobioscience: Department of Life and Environmental System Science Graduate School of Data Science Graduate School of Data Science: Department of Data Science Graduate School of Data Science: Department of Health Data Science Graduate School of Medical Life Science Graduate School of Medicine Graduate School of Medicine: Department of Medicine Graduate School of Medicine: Department of Nursing Non-Degree Programs Exchange Program International Clinical Clerkship Research-Only Career Development Support Admissions Research Advanced Medical Research Center Kihara Institute for Biological Research Life at YCU Kanazawa-Hakkei Campus Life Fukuura Campus Life Living in Yokohama Clubs &＃038; Societies Health &＃038; Wellness Global International Affairs Office Exchange Program Partner Institutions Global Cooperation Institute for Sustainable Cities (GCI) 日本語 Seasonal pigment fluctuation in diploid and polyploid Arabidopsis revealed by machine learning-based phenotyping method PlantServation2023-09-22Event Report: The 14th IACSC International Symposium/General Assembly2023-10-10 Show all Combination of Sacubitril/Valsartan and Blockade of the PI3K Pathway Enhanced Kidney Protection in a Mouse Model of Cardiorenal Syndrome Date: 29 Sep 23 Researcher(s): Hiromichi Wakui,Shunichiro Tsukamoto Aims Angiotensin receptor-neprilysin inhibitor (ARNI) is an established treatment for heart failure. However, whether ARNI has renoprotective effects beyond renin-angiotensin system inhibitors alone in cardiorenal syndrome (CRS) has not been fully elucidated. Here, we examined the effects of ARNI on the heart and kidneys of CRS model mice with overt albuminuria and identified the mechanisms underlying ARNI-induced kidney protection. Methods and results C57BL6 mice were subjected to chronic angiotensin II infusion, nephrectomy, and salt loading (ANS); they developed CRS phenotypes and were divided into the vehicle treatment (ANS-vehicle), sacubitril/valsartan treatment (ANS-ARNI), and two different doses of valsartan treatment (ANS-VAL M, ANS-VAL H) groups. Four weeks after treatment, the hearts and kidneys of each group were evaluated. The ANS-vehicle group showed cardiac fibrosis, cardiac dysfunction, overt albuminuria, and kidney fibrosis. The ANS-ARNI group showed a reduction in cardiac fibrosis and cardiac dysfunction compared with the valsartan treatment groups. However, regarding the renoprotective effects characterized by albuminuria and fibrosis, ARNI was less effective than valsartan. Kidney transcriptomic analysis showed that the ANS-ARNI group exhibited a significant enhancement in the phosphoinositide 3-kinase (PI3K)-AKT signalling pathway compared with the ANS-VAL M group. Adding PI3K inhibitor treatment to ARNI ameliorated kidney injury to levels comparable with those of ANS-VAL M while preserving the superior cardioprotective effect of ARNI. Conclusion PI3K pathway activation has been identified as a key mechanism affecting remnant kidney injury under ARNI treatment in CRS pathology, and blockading the PI3K pathway with simultaneous ARNI treatment is a potential therapeutic strategy for treating CRS with overt albuminuria. Link to full article For inquiries regarding this press release Shunichiro TsukamotoDepartment of Medical Science and Cardiorenal Medicine, Yokohama City University Graduate School of Medicine, Yokohama, Japan Hiromichi WakuiAssociate Professor Department of Medical Science and Cardiorenal Medicine, Yokohama City University Graduate School of Medicine, 3-9 Fukuura, Kanazawa-ku, Yokohama 236-0004, Japan. 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