Laboratories

Immunometabolism

KEYWORDS

  • Chronic inflammation
  • Obesity
  • MASH
  • Metabolism
  • Nutrition
  • Macrophage
  • Cell death
  • Fibrosis

HEAD

SUGANAMI Takayoshi

Professor

LAB MEMBER

Faculty Position Researchers
TANAKA Miyako Lecturer
ITO Ayaka Lecturer

CONTACT

Email iga-ryu◎t.mail.nagoya-u.ac.jp (Please send a message after replacing "◎" mark with "@" mark. )
HP Private Page

OUTLINE

With the Westernization of lifestyles, obesity has been increasing in Japan, contributing to metabolic syndrome and various lifestyle-related diseases. Lifestyle-related diseases are typical multifactorial disorders that arise from interactions between genetic predisposition and environmental factors, and are significantly influenced by changes in our surrounding environment. In our laboratory, we aim to elucidate the molecular mechanisms underlying lifestyle-related diseases by understanding not only individual molecules or cells, but also the interactions among diverse cell types within each organ and the inter-organ networks.
As a key concept for understanding lifestyle-related diseases, we focus on ""immunometabolism."" Recent evidence has shown that lifestyle-related diseases, traditionally regarded as metabolic disorders, also possess characteristics of chronic inflammatory diseases. We are investigating how overnutrition induces chronic inflammation and whether interventions targeting chronic inflammation can lead to treatments for lifestyle-related diseases. In addition to these pathophysiological studies, we have recently been developing novel therapeutic approaches with medical-engineering collaborations. Through these efforts, our laboratory seeks to contribute to elucidating the pathophysiology of lifestyle-related diseases and developing new treatments, positioning ourselves at the interface between basic and clinical research.

RESEARCH PROJECTS

1.Elucidation of mechanisms underlying cell death-triggered chronic inflammation

  • Adipose tissue undergoes substantial structural changes during the progression of obesity; discovery of molecules that regulate adipose tissue function through intercellular interactions
    Diabetes 74: 1135-1152, 2025 (Selected as Paper of the Month)
  • Mechanisms of the AKI-to-CKD transition mediated by Mincle, a dead cell sensor; potential for developing novel preventive strategies for CKD
    J. Exp. Med. 217: e20192230, 2020
  • Elucidation of novel pathogenic mechanisms of MASH; through the development of a novel MASH disease model
    JCI Insight 2: e92902, 2017
  • Discovery of key molecules causing adipose tissue fibrosis associated with obesity; a novel molecular target for metabolic syndrome treatment
    Nat. Commun. 5: 4982, 2014

2. Intracellular metabolism and chronic inflammation

  • Elucidation of novel pathogenic mechanisms of MASH; iron accumulation in Kupffer cells promotes liver fibrosis
    iScience 24: 102032, 2021
  • EPA intake suppresses plasma cell differentiation and ameliorates systemic lupus erythematosus pathology
    Front. Immunol. 12: 650856, 2021

3. Development of novel therapeutic strategies through medical-engineering collaborations

  • - Cholesterol accumulation in macrophages promotes liver fibrosis; toward the development of MASH therapy using supramolecular polyrotaxane
    J. Exp. Med. 220: e20220681, 2023
  • Development of an ""electronics-free"" artificial pancreas device; autonomous insulin release in response to blood glucose changes
    Sci. Adv. 3: eaaq0723, 2017

BIBLIOGRAPHY

2025
  1. H. Kohda, M. Tanaka, S. Shichino, S. Arakawa, T. Komori, A. Ito, E. Wada, K. Ochi, X. Yuan, T. Takeda, A. Saiki, I. Tatsuno, K. Ikeda, Y. Miyai, A. Enomoto, Y. Morikawa, S. Shimizu, S. Ueha, K. Matsushima, Y. Ogawa, T. Suganami. Novel Cell-to-Cell Communications Between Macrophages and Fibroblasts Regulate Obesity-Induced Adipose Tissue Fibrosis. Diabetes 74: 1135-1152, 2025.
  2. E. Wada, H. Hosono, M. Tanaka, F. Miyakawa, K. Ochi, H. Kohda, S. Tanno, R. Shimano, A. Ito, Y. Kitaura, K. Ichihara, A. Matsumoto, T. Ogi, N. Satoh-Asahara, Y. Murohara, *T. Suganami. Transient dietary intervention induces healthy adipose tissue expansion and metabolically healthy obesity in mice. FASEB J. 39: e70847, 2025.
2023
  1. M. Itoh, A. Tamura, S. Kanai, M. Tanaka, Y. Kanamori, I. Shirakawa, A. Ito, Y. Oka, I. Hidaka, T. Takami, Y. Honda, M. Maeda, Y. Saito, Y. Murata, T. Matozaki, A. Nakajima, Y. Kataoka, T. Ogi, Y. Ogawa, T. Suganami. Lysosomal cholesterol overload in macrophages promotes liver fibrosis in a mouse model of NASH. J. Exp. Med. 220: e20220681, 2023.
2021
  1. A. Kobayashi, A. Ito, I. Shirakawa, A. Tamura, S. Tomono, H. Shindou, P. Niklas Hedde, M. Tanaka, N. Tsuboi, T. Ishimoto, S. Akashi-Takamura, S. Maruyama, T. Suganami. Dietary supplementation with eicosapentaenoic acid inhibits plasma cell differentiation and attenuates lupus autoimmunity. Front. Immunol. 12: 650856, 2021.
  2. Y. Kanamori, M. Tanaka, M. Itoh, K. Ochi, A. Ito, I. Hidaka, I. Sakaida, Y. Ogawa, T. Suganami. Iron-rich Kupffer cells exhibit phenotypic changes during the development of liver fibrosis in NASH. iScience 24: 102032, 2021.
2020
  1. M. Tanaka, M. Saka-Tanaka, K. Ochi, K. Fujieda, Y. Sugiura, T. Miyamoto, H. Kohda, A. Ito, T. Miyazawa, A. Matsumoto, S. Aoe, Y. Miyamoto, N. Tsuboi, S. Maruyama, M. Suematsu, S. Yamasaki, Y. Ogawa, T. Suganami. C-type lectin Mincle mediates cell death–triggered sustained inflammation in acute kidney injury. J. Exp. Med. 217: e20192230, 2020.
  2. A. Matsumoto, H. Kuwata, S. Kimura, H. Matsumoto, K. Ochi, Y. Moro-oka, A. Watanabe, H. Yamada, H. Ishii, T. Miyazawa, S. Chen, T. Baba, H. Yoshida, T. Nakamura, H. Inoue, Y. Ogawa, M. Tanaka, Y. Miyahara, T. Suganami. Hollow fiber-combined glucose-responsive gel technology as an in vivo electronics-free insulin delivery system. Commun. Biol. 3: 313, 2020.
2017
  1. A. Matsumoto, M. Tanaka, H. Matsumoto, K. Ochi, Y. Moro-oka, H. Kuwata, H. Yamada, I. Shirakawa, T. Miyazawa, H. Ishii, K. Kataoka, Y. Ogawa, Y. Miyahara, T. Suganami. Synthetic “smart-gel” provides glucose-responsive insulin delivery in diabetic mice. Sci. Adv. 3: eaaq0723, 2017. (cover picture of the issue)
  2. M. Itoh, T. Suganami, H. Kato, S. Kanai, I. Shirakawa, T. Sakai, T. Goto, M. Asakawa, I. Hidaka, H. Sakugawa, K. Ohnishi, Y. Komohara, K. Asano, I. Sakaida, M. Tanaka, Y. Ogawa. CD11c-positive resident macrophages drive hepatocyte death-triggered liver fibrosis in a murine model of non-alcoholic steatohepatitis. JCI Insight 2: e92902, 2017.
2014
  1. M. Tanaka, K. Ikeda, T. Suganami, C. Komiya, K. Ochi, I. Shirakawa, M. Hamaguchi, S. Nishimura, I. Manabe, T. Matsuda, K. Kimura, H. Inoue, Y. Inagaki, S. Aoe, S. Yamasaki, Y. Ogawa. Macrophage-inducible C-type lectin underlies obesity-induced adipose tissue fibrosis. Nat. Commun. 5: 4982, 2014.

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