Tokushima University / Educator and Researcher Directory --- Shiozaki, Yuji

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Book:

1.	Masashi Masuda, Yuji Shiozaki and Makoto Miyazaki : Chapter 10 - Lipotoxicity in the pathogenesis of chronic kidney disease complications, Academic Press, Aug. 2023. (Link to Publication Site) ● Publication site (DOI): 10.1016/C2021-0-02221-5 (Link to Search Site for Scientific Articles) ● Search Scopus @ Elsevier (DOI): 10.1016/C2021-0-02221-5 (DOI: 10.1016/C2021-0-02221-5)
2.	Hiroko Segawa, 小池萌, Yuji Shiozaki and Ken-ichi Miyamoto : 抗老化因子を制御するミネラル栄養学-リン代謝恒常制御の重要性., Apr. 2022.

Academic Paper (Judged Full Paper):

1.	Shinobu Miyazaki-Anzai, Masashi Masuda, Audrey L Keenan, Yuji Shiozaki, Jose G Miranda and Makoto Miyazaki : Activation of the IKK2/NF-κB pathway in VSMCs inhibits calcified vascular stiffness in CKD, JCI Insight, Vol.9, No.7, 12:e174977, 2024. (Summary) IKK2/NF-κB pathway-mediated inflammation in vascular smooth muscle cells (VSMCs) has been proposed to be an etiologic factor in medial calcification and stiffness. However, the role of the IKK2/NF-κB pathway in medial calcification remains to be elucidated. In this study, we found that chronic kidney disease (CKD) induces inflammatory pathways through the local activation of the IKK2/NF-κB pathway in VMSCs associated with calcified vascular stiffness. Despite reducing the expression of inflammatory mediators, complete inhibition of the IKK2/NF-κB pathway in vitro and in vivo unexpectedly exacerbated vascular mineralization and stiffness. In contrast, activation of NF-κB by SMC-specific IκBα deficiency attenuated calcified vascular stiffness in CKD. Inhibition of the IKK2/NF-κB pathway induced cell death of VSMCs by reducing anti-cell death gene expression, whereas activation of NF-κB reduced CKD-dependent vascular cell death. In addition, increased calcification of extracellular vesicles through the inhibition of the IKK2/NF-κB pathway induced mineralization of VSMCs, which was significantly reduced by blocking cell death in vitro and in vivo. This study reveals that activation of the IKK2/NF-κB pathway in VSMCs plays a protective role in CKD-dependent calcified vascular stiffness by reducing the release of apoptotic calcifying extracellular vesicles. (Keyword) Humans / NF-kappa B / Signal Transduction / Vascular Stiffness / Muscle, Smooth, Vascular / Renal Insufficiency, Chronic (Tokushima University Institutional Repository) ● Metadata: 119162 (Link to Publication Site) ● Publication site (DOI): 10.1172/jci.insight.174977 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 38470493 ● Search Scopus @ Elsevier (PMID): 38470493 ● Search Scopus @ Elsevier (DOI): 10.1172/jci.insight.174977 (Tokushima University Institutional Repository: 119162, DOI: 10.1172/jci.insight.174977, PubMed: 38470493)
2.	Megumi Koike, Tetsuhiko Sato, Yuji Shiozaki, Aoi Komiya, Mizuki Miura, Ayami Higashi, Akane Ishikawa, Kaori Takayanagi, Minori Uga, Ken-ichi Miyamoto and Hiroko Segawa : Involvement of α-klotho in growth hormone (GH) signaling, Journal of Clinical Biochemistry and Nutrition, Vol.74, No.3, 221-229, 2024. (Keyword) growth hormone / α-klotho / kidney / CKD / GH-resistant (Tokushima University Institutional Repository) ● Metadata: 119161 (Link to Publication Site) ● Publication site (DOI): 10.3164/jcbn.23-127 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1390581468909331072 ● Search Scopus @ Elsevier (DOI): 10.3164/jcbn.23-127 (Tokushima University Institutional Repository: 119161, DOI: 10.3164/jcbn.23-127, CiNii: 1390581468909331072)
3.	Kazuya Tanifuji, Yuji Shiozaki, Megumi Koike, Minori Uga, Mizuki Miura, Ayami Higashi, Takaaki Shimohata, Akira Takahashi, Hisayoshi Hayashi, Noriko Ishizuka, Yasuhiro Ichida, Shuichi Ohtomo, Naoshi Horiba, Ken-ichi Miyamoto and Hiroko Segawa : Effects of EOS789, a novel pan-phosphate transporter inhibitor, on phosphate metabolism : Comparison with a conventional phosphate binder, The Journal of Medical Investigation : JMI, Vol.70, No.1,2, 260-270, 2023. (Summary) Inorganic phosphate (Pi) binders are the only pharmacologic treatment approved for hyperphosphatemia. However, Pi binders induce the expression of intestinal Pi transporters and have limited effects on the inhibition of Pi transport. EOS789, a novel pan-Pi transporter inhibitor, reportedly has potent efficacy in treating hyperphosphatemia. We investigated the properties of EOS789 with comparison to a conventional Pi binder. Protein and mRNA expression levels of Pi transporters were measured in intestinal and kidney tissues from male Wistar rats fed diets supplemented with EOS789 or lanthanum carbonate (LC). 32Pi permeability was measured in intestinal tissues from normal rats using a chamber. Increased protein levels of NaPi-2b, an intestinal Pi transporter, and luminal Pi removal were observed in rats treated with LC but not in rats treated with EOS789. EOS789 but not LC suppressed intestinal protein levels of the Pi transporter Pit-1 and sodium/hydrogen exchanger isoform 3. 32Pi flux experiments using small intestine tissues from rats demonstrated that EOS789 may affect transcellular Pi transport in addition to paracellular Pi transport. EOS789 has differing regulatory effects on Pi metabolism compared to LC. The properties of EOS789 may compensate for the limitations of LC therapy. The combined or selective use of EOS789 and conventional Pi binders may allow tighter control of hyperphosphatemia. J. Med. Invest. 70 : 260-270, February, 2023. (Keyword) Rats / Male / Animals / Phosphate Transport Proteins / Rats, Wistar / Hyperphosphatemia / Intestinal Absorption / Phosphates (Tokushima University Institutional Repository) ● Metadata: 118209 (Link to Publication Site) ● Publication site (DOI): 10.2152/jmi.70.260 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 37164731 ● Search Scopus @ Elsevier (PMID): 37164731 ● Search Scopus @ Elsevier (DOI): 10.2152/jmi.70.260 (Tokushima University Institutional Repository: 118209, DOI: 10.2152/jmi.70.260, PubMed: 37164731)
4.	Sumire Sasaki, Yuji Shiozaki, Ai Hanazaki, Megumi Koike, Kazuya Tanifuji, Minori Uga, Kota Kawahara, Ichiro Kaneko, Yasuharu Kawamoto, Pattama Wiriyasermkul, Tomoka Hasegawa, Norio Amizuka, Ken-ichi Miyamoto, Shushi Nagamori, Yoshikatsu Kanai and Hiroko Segawa : Tmem174, a regulator of phosphate transporter prevents hyperphosphatemia., Scientific Reports, Vol.12, No.1, 2022. (Summary) Renal type II sodium-dependent inorganic phosphate (Pi) transporters NaPi2a and NaPi2c cooperate with other organs to strictly regulate the plasma Pi concentration. A high Pi load induces expression and secretion of the phosphaturic hormones parathyroid hormone (PTH) and fibroblast growth factor 23 (FGF23) that enhance urinary Pi excretion and prevent the onset of hyperphosphatemia. How FGF23 secretion from bone is increased by a high Pi load and the setpoint of the plasma Pi concentration, however, are unclear. Here, we investigated the role of Transmembrane protein 174 (Tmem174) and observed evidence for gene co-expression networks in NaPi2a and NaPi2c function. Tmem174 is localized in the renal proximal tubules and interacts with NaPi2a, but not NaPi2c. In Tmem174-knockout (KO) mice, the serum FGF23 concentration was markedly increased but increased Pi excretion and hypophosphatemia were not observed. In addition, Tmem174-KO mice exhibit reduced NaPi2a responsiveness to FGF23 and PTH administration. Furthermore, a dietary Pi load causes marked hyperphosphatemia and abnormal NaPi2a regulation in Tmem174-KO mice. Thus, Tmem174 is thought to be associated with FGF23 induction in bones and the regulation of NaPi2a to prevent an increase in the plasma Pi concentration due to a high Pi load and kidney injury. (Keyword) Animals / Fibroblast Growth Factors / hyperphosphatemia / hypophosphatemia / Membrane Proteins / knockout mice / Parathyroid Hormone / Phosphate Transport Proteins / Phosphates (Link to Publication Site) ● Publication site (DOI): 10.1038/s41598-022-10409-3 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 35428804 ● Search Scopus @ Elsevier (PMID): 35428804 ● Search Scopus @ Elsevier (DOI): 10.1038/s41598-022-10409-3 (DOI: 10.1038/s41598-022-10409-3, PubMed: 35428804)
5.	Sumire Sasaki, Megumi Koike, Kazuya Tanifuji, Minori Uga, Kota Kawahara, Aoi Komiya, Mizuki Miura, Yamato Harada, Yuki Hamaguchi, Shohei Sasaki, Yuji Shiozaki, Ichiro Kaneko, Ken-ichi Miyamoto and Hiroko Segawa : Dietary polyphosphate has a greater effect on renal damage and FGF23 secretion than dietary monophosphate, The Journal of Medical Investigation : JMI, Vol.69, No.3, 173-179, 2022. (Summary) Phosphate (Pi)-containing food additives are used in several forms. Polyphosphate (PPi) salt has more harmful effects than monophosphate (MPi) salt on bone physiology and renal function. This study aimed to analyze the levels of parathyroid hormone PTH and fibroblast growth factor 23 (FGF23) and the expression of renal / intestinal Pi transport-related molecules in mice fed with an MPi or PPi diet. There were no significant differences in plasma Pi concentration and fecal Pi excretion levels between mice fed with the high-MPi and PPi diet. However, more severe tubular dilatation, interstitial fibrosis, and calcification were observed in the kidneys of mice fed with the high PPi diet versus the MPi diet. Furthermore, there was a significant increase in serum FGF23 levels and a decrease in renal phosphate transporter protein expression in mice fed with the PPi diet versus the MPi diet. Furthermore, the high MPi diet was associated with significantly suppressed expression and activity of intestinal alkaline phosphatase protein. In summary, PPi has a more severe effect on renal damage than MPi, as well as induces more FGF23 secretion. Excess FGF23 may be more involved in inflammation, fibrosis, and calcification in the kidney. J. Med. Invest. 69 : 173-179, August, 2022. (Keyword) Animals / Mice / Alkaline Phosphatase / Diet / Fibroblast Growth Factors / Fibrosis / Food Additives / Kidney / Parathyroid Hormone / Phosphate Transport Proteins / Phosphates / Polyphosphates (Tokushima University Institutional Repository) ● Metadata: 117148 (Link to Publication Site) ● Publication site (DOI): 10.2152/jmi.69.173 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 36244766 ● Summary page in Scopus @ Elsevier: 2-s2.0-85139886601 (Tokushima University Institutional Repository: 117148, DOI: 10.2152/jmi.69.173, PubMed: 36244766, Elsevier: Scopus)

Academic Paper (Unrefereed Paper):

1.	Masashi Masuda, Yuji Shiozaki, Yutaka Taketani and 宮崎淳 : 最前線慢性腎臓病の合併症とlipotoxicity, Farumashia, Vol.58, No.4, 329-333, 2022. (Tokushima University Institutional Repository) ● Metadata: 118681 (Link to Publication Site) ● Publication site (DOI): 10.14894/faruawpsj.58.4_329 (Link to Search Site for Scientific Articles) ● Search Scopus @ Elsevier (DOI): 10.14894/faruawpsj.58.4_329 (Tokushima University Institutional Repository: 118681, DOI: 10.14894/faruawpsj.58.4_329)
2.	金子一郎, 宇賀穂, Yuji Shiozaki, Ken-ichi Miyamoto and Hiroko Segawa : The physiological function of vitamin D which maintains phosphate homeostasis, Vitamins, Vol.95, No.56, 280-285, 2021. (Summary) Inorganic phosphate (Pi) plays essential roles in many biological processes. Blood Pi level should be maintained at a constant range because hypophosphatemia causes rickets/osteomalacia, whereas hyperphosphatemia causes cardiovascular events in chronic kidney disease (CKD) or hemodialysis patients. As a phosphaturic hormone, parathyroid hormone (PTH) or fibroblast growth factor (FGF) 23 strongly suppresses Pi reabsorption. 1,25-Dihydroxyvitamin D[1,25(OH) <sub>2</sub>D] up-regulates Pi absorption in intestines, and regulates urinary Pi excretion through PTH or FGF23. <br> Activated FGF23 signal leads urinary Pi excretion, and hypophosphatemic rickets (FGF23-related hypophosphatemic rickets). Rickets characterized as vitamin D deficiency also associates with impaired renal Pi reabsorption in juvenile stage in addition to low Pi absorption in intestines. Now, burosumab (FGF23 neutralizing antibody) has a beneficent effect on FGF23-related hypophosphatemic rickets/osteomalacia. The antibody increases renal Pi reabsorption and 1,25(OH) <sub>2</sub>D production. On the other hand, treatment with vitamin D alone in an animal model of X-linked hypophosphatemic rickets can potentially increase renal Pi reabsorption, despite of excess FGF23, and improve hypophosphatemia and bone phenotypes. <br> CKD patients often accompany with mineral bone disorder (CKD-MBD) such as hyperparathyroidism, cardiovascular calcification, and osteodystrophy. Prevention and treatment for hyperphosphatemia or hypovitaminosis D would improve their QOL or mortality. <br> Thus, renal Pi reabsorption is important for bone and mineral homeostasis. We focus on the metabolism of Pi and vitamin D to understand the molecular mechanism for the onset and prevention of diseases associated with Pi and vitamin D. (Keyword) Phosphate / Vitamin D / VDR / Rickets / CKD (Link to Publication Site) ● Publication site (DOI): 10.20632/vso.95.5-6_280 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1390574047045835904 ● Search Scopus @ Elsevier (DOI): 10.20632/vso.95.5-6_280 (DOI: 10.20632/vso.95.5-6_280, CiNii: 1390574047045835904)

Review, Commentary:

1.	Megumi Koike, Ayami Higashi, Aoi Komiya, Yuji Shiozaki and Hiroko Segawa : リン管理―CKD-MBDと栄養, Kidney and Dialysis, Vol.96, No.1, 112-116, Jan. 2024. (Link to Publication Site) ● Publication site (DOI): 10.24479/kd.0000001175 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1390580793827920896 ● Search Scopus @ Elsevier (DOI): 10.24479/kd.0000001175 (DOI: 10.24479/kd.0000001175, CiNii: 1390580793827920896)
2.	Megumi Koike, Yuji Shiozaki and Hiroko Segawa : 無機リン酸の恒常性維持, Kidney and Dialysis, Vol.95, No.3, 267-271, Sep. 2023. (Link to Publication Site) ● Publication site (DOI): 10.24479/kd.0000000864 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1390860620061733888 ● Search Scopus @ Elsevier (DOI): 10.24479/kd.0000000864 (DOI: 10.24479/kd.0000000864, CiNii: 1390860620061733888)
3.	Megumi Koike, Minori Uga, Yuji Shiozaki, Ken-ichi Miyamoto and Hiroko Segawa : Regulation of Phosphate Transporters and Novel Regulator of Phosphate Metabolism, Endocrines, Vol.4, No.3, 607-615, Aug. 2023. (Link to Publication Site) ● Publication site (DOI): 10.3390/endocrines4030043 (Link to Search Site for Scientific Articles) ● Search Scopus @ Elsevier (DOI): 10.3390/endocrines4030043 (DOI: 10.3390/endocrines4030043)
4.	谷藤和也, 小池萌, 宇賀稔, Yuji Shiozaki and Hiroko Segawa : Ca，Pホメオスタシス, Kidney and Dialysis, Vol.93, No.5, 736-741, Nov. 2022. (Keyword) PTH / FGF23 / CaSR (Link to Publication Site) ● Publication site (DOI): 10.24479/kd.0000000375 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1390577133295330048 ● Search Scopus @ Elsevier (DOI): 10.24479/kd.0000000375 (DOI: 10.24479/kd.0000000375, CiNii: 1390577133295330048)
5.	Hiroko Segawa, Megumi Koike, Yuji Shiozaki and Ken-ichi Miyamoto : 抗老化因子を制御するミネラル栄養学-リン代謝恒常制御の重要性, 実験医学増刊∼栄養・代謝物シグナルと食品機能∼, Vol.40, No.7, 45-50, Mar. 2022.
6.	谷藤和也, Yuji Shiozaki and Hiroko Segawa : 骨を維持する栄養素, Journal of Health, Physical Education and Recreation, Vol.71, No.11, 801-806, Nov. 2021. (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1520572360407947392 (CiNii: 1520572360407947392)

Proceeding of International Conference:

1.	Yuji Shiozaki, Minori Uga, Mizuki Miura, Aoi Komiya, Kazuya Tanifuji, Megumi Koike, Ken-ichi Miyamoto and Hiroko Segawa : Analysis of regulation of Tmem174 expression by Pi concentration and PTH signaling in opossum kidney cells., Physiology, Biology and Pathology of Phosphate Gordon Research Conference, Grand Galvez in Galveston, Texas, United States, Feb. 2023.
2.	Uga Minori, Ichiro Kaneko, Sasaki Sumire, Koike Megumi, Tanifuji Kazuya, Yuji Shiozaki, Jurutka W. Peter and Hiroko Segawa : The role of intestinal Cytochrome P450 in vitamin D metabolism, 22nd International Congress of Nutrition in Tokyo, Dec. 2022.

Proceeding of Domestic Conference:

1.	KOMIYA Aoi, Megumi Koike, UGA Minori, Ayami Higashi, ISHIKAWA Akane, SHIBAHARA Shion, Yuji Shiozaki, Ken-ichi Miyamoto and Hiroko Segawa : NEP25 Tgマウス CKD-MBDモデルを用いた新規リン代謝調節機構の解明, 第9回日本栄養改善学会四国支部学術総会, Jun. 2024.
2.	Megumi Koike, Ayami Higashi, KOMIYA Aoi, Yuji Shiozaki, UGA Minori, SHIBAHARA Shion, Ken-ichi Miyamoto and Hiroko Segawa : 成長を制御する新規システム-ミネラル代謝・抗老化因子 α-klotho-, 第78回日本栄養・食糧学会大会, May 2024.
3.	Yuji Shiozaki, YUKI Hamaguchi, UGA Minori, SHIBAHARA Shion, KOMIYA Aoi, Ayami Higashi, ISHIKAWA Akane, Megumi Koike, Ken-ichi Miyamoto and Hiroko Segawa : 腎臓リン酸再吸収機構におけるリン酸排出トランスポーターXpr1の役割, 第78回日本栄養・食糧学会大会, May 2024.
4.	Yamato Harada, Minori Uga, Aoi Komiya, Mizuki Miura, Ayami Higashi, Akane Ishikawa, Shion Shibahara, Megumi Koike, Yuji Shiozaki and Hiroko Segawa : 新規リン代謝調節因子Tmem174の血中リン濃度調節における役割, 第7回日本Uremic Toxin研究会学術集会, Apr. 2024.
5.	Yuji Shiozaki : Tmem174によるNaPi2a制御についての最新知見, 第8回CKD-MBD学会学術集会・総会, Mar. 2024.
6.	Minori Uga, Yuji Shiozaki, Aoi Komiya, Mizuki Miura, Yamato Hrada, Ayami Higashi, Akane Ishikawa, Megumi Koike, Ken-ichi Miyamoto, Yoshikatsu Kanai and Hiroko Segawa : リン代謝調節因子Tmem174によるNaPi2a内在化機序の解明, 第56回日本栄養・食糧学会中国・四国支部大会, Oct. 2023.
7.	Aoi Komiya, miura mizuki, Megumi Koike, Minori Uga, Yuki Hamaguchi, YAMATO Harada, Ayami Higashi, ISHIKAWA Akane, Yuji Shiozaki, Ken-ichi Miyamoto and Hiroko Segawa : リン感受センサーの探索, 第70回日本栄養改善学会学術総会, Sep. 2023.
8.	Minori Uga, Sumire Sasaki, Mizuki Miura, Yamato Hrada, Aoi Komiya, Ayami Higashi, Akane Ishikawa, Megumi Koike, Yuji Shiozaki, Yoshikatsu Kanai, Ken-ichi Miyamoto and Hiroko Segawa : 高リン血症を予防する新規リン代謝調節因子の同定, 第267回徳島医学会学術集会, Aug. 2023.
9.	Miura Mizuki, Sumire Sasaki, Yuji Shiozaki, Megumi Koike, Minori Uga, Ayami Higashi, 長谷川智香, 網塚憲生, Ken-ichi Miyamoto and Hiroko Segawa : Tmem174はリン酸トランスポーターを調節し高リン血症を予防する新規リン代謝調節分子である, 第41回日本骨代謝学会学術集会, Jul. 2023.
10.	uga Minori, Yuji Shiozaki, Miura Mizuki, Komiya Aoi, Harada Yamato, KOIKE Megumi, Ken-ichi Miyamoto and Hiroko Segawa : Regulatory mechanism of Tmem174, a novel factor of phosphate homeostasis, 第77回日本栄養・食糧学会大会, May 2023.
11.	Yuji Shiozaki, YUKI Hamaguchi, Mana Muramoto, TANIFUJI Kazuya, Uga Minori, MIZUKI Miura, AOI Komiya, KOIKE Megumi, Ken-ichi Miyamoto and Hiroko Segawa : XPR1, a phosphate exporter, represses high Pi loading-induced toxicity., 第77回日本栄養・食糧学会大会, May 2023.
12.	MIZUKI Miura, Sumire Sasaki, Yuji Shiozaki, TANIFUJI Kazuya, KOIKE Megumi, UGA Minori, Ken-ichi Miyamoto and Hiroko Segawa : Tmem174 はリン酸トランスポーターを調節し高リン血症を予防する., 第7回日本CKD-MBD学会学術集会・総会, Mar. 2023.
13.	Sumire Sasaki, Yuji Shiozaki, KOIKE Megumi, TANIFUJI Kazuya, UGA Minori, Ken-ichi Miyamoto and Hiroko Segawa : Tmem174はリン酸トランスポーターを調節し高リン血症を予防する, 第95回日本生化学会大会, Nov. 2022.
14.	MIZUKI Miura, Sumire Sasaki, KOIKE Megumi, TANIFUJI Kazuya, UGA Minori, AOI Komiya, YUKI Hamaguchi, YAMATO Harada, Yuji Shiozaki, Ken-ichi Miyamoto and Hiroko Segawa : ポリリン酸は，モノリン酸よりも腎障害およびFGF23分泌に大きな影響を与える, 第69回日本栄養改善学会学術総会, Sep. 2022.
15.	Hiroko Segawa, Yuji Shiozaki, Ichiro Kaneko and Ken-ichi Miyamoto : リンが関する生体機能ー成長，疾患，寿命ー, 第76回日本栄養・食糧学会大会シンポジウム 4 ミネラルの新機能, Jun. 2022.
16.	宇賀穂, 金子一郎, 佐々木すみれ, 小池萌, 谷藤和也, 川原滉太, 小宮蒼, 原田和, 浜口ゆき, 三浦美月, Yuji Shiozaki and Hiroko Segawa : 小腸Cytochrome P450(CYP3A)がビタミンD活性に及ぼす影響, 第54回日本栄養・食糧学会中国・四国支部大会・第7回日本栄養改善学会四国支部学術総会合同大会, Oct. 2021.
17.	川原滉太, 小池萌, 佐々木すみれ, 谷藤和也, Yuji Shiozaki, 金子一郎 and Hiroko Segawa : ライフステージに着目した生体内リン代謝の性差検討, 第68回日本栄養改善学会学術総会, Oct. 2021.
18.	川原滉太, 小池萌, 佐々木すみれ, 谷藤和也, Yuji Shiozaki, 金子一郎 and Hiroko Segawa : ライフステージに着目した生体内リン代謝の性差検討, 第75回日本栄養・食糧学会大会, Jul. 2021.

Et cetera, Workshop:

1.	Yuji Shiozaki, miura mizuki, uga minori, komiya aoi, harada yamato, higashi ayami, koike megumi, Ken-ichi Miyamoto and Hiroko Segawa : 高リン血症予防に関与する新規リン代謝調節因子Transmembrane protein (Tmem) 174の同定, 第6回日本Uremic Toxin研究会学術集会, May 2023.
2.	Yuji Shiozaki and Hiroko Segawa : 腎リン酸トランスポーターの機能制御と疾患, 第16回トランスポーター研究会年会, Jul. 2022.
3.	Yuji Shiozaki, 佐々木すみれ, 小池萌, 谷藤和也, 川原滉太, 浜口ゆき, 金子一郎, Ken-ichi Miyamoto and Hiroko Segawa : 近位尿細管細胞分化におけるリン酸トランスポーターNaPi-IIcの役割, 第1回トランスポーター研究会関西西部会JTRAKansai2021∼トランスポーター研究の架け橋∼, Oct. 2021.

Grants-in-Aid for Scientific Research (KAKEN Grants Database @ NII.ac.jp)

リン酸排出トランスポーター制御による寝たきり予防：破骨細胞とリン動態の解析 (Project/Area Number: 24K14626 )
細胞内リン酸排出分子XPR1による抗組織老化作用の解明 (Project/Area Number: 22K17800 )
小腸FGF19産生・分泌を基盤とした健康長寿を目指す栄養療法 (Project/Area Number: 21K11594 )
抗老化因子を制御するミネラル栄養学の確立 (Project/Area Number: 21H03375 )
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