Laboratories

Disease Control

KEYWORDS

  • Fibrosis
  • Myofibroblast

HEAD

NAKAYA Michio

Professor

Researchers

LAB MEMBER

Faculty Position Researchers
SUZUKI Hiromi Assistant Professor Researchers

CONTACT

Email nakaya◎riem.nagoya-u.ac.jp (Please send a message after replacing "◎" mark with "@" mark. )
HP Private Page

OUTLINE

Fibrosis is a pathological condition characterized by the excessive accumulation of extracellular matrix (ECM) proteins, such as collagen, within tissues. Fibrosis is observed in a wide range of highly prevalent diseases, including cardiac hypertrophy, pulmonary fibrosis, chronic renal failure, fatty liver disease, and even refractory cancers, where it contributes to disease progression and worsening of pathology. Indeed, fibrosis is estimated to be involved in approximately 45% of all deaths in developed countries. Despite its enormous clinical impact, there are currently no definitive strategies to control fibrosis, and the development of breakthrough anti-fibrotic therapies and drugs is urgently needed.
Tissue fibrosis is executed by a specialized population of cells known as myofibroblasts, which are responsible for the excessive production of extracellular matrix proteins such as collagen. Myofibroblasts are absent in healthy tissues and arise through the differentiation of resident fibroblasts in response to inflammatory stimuli. Our research aims to identify novel molecular regulators that control the collagen-producing capacity of myofibroblasts and to develop innovative anti-fibrotic therapies and drugs by targeting these molecules.

RESEARCH PROJECTS

  1. Exploration and Identification of Novel Pro-fibrotic Molecules and Their Therapeutic Applications
  2. Identification of Molecular Determinants Defining Myofibroblast Subpopulations
  3. Analysis of Myofibroblast Fate and Lifespan
  4. 2025 Disease Control Science – Field Overview

BIBLIOGRAPHY

2025
  1. Mieno H, Nakaya M. [Myofibroblast differentiation induced by mechanical stimulation]. Nihon Yakurigaku Zasshi. 2025;160(3):221. Japanese. doi: 10.1254/fpj.25016. PMID: 40307053.
  2. 「線維化のメカノバイオロジー」渡邊颯人, 仲矢道雄　医学のあゆみ in press (2025)
  3. 三重野博貴, 仲矢道雄「機械的刺激による筋線維芽細胞の性質変化」日本薬理学雑誌　160(3):221. (2025)
2024
  1. Yamauchi Y, Mieno H, Suetsugu H, Watanabe H, Nakaya M. Elevated PRELP expression in heart and liver fibrosis promotes collagen production. Biochem Biophys Res Commun. 2024 Nov 19;734:150785. doi: 10.1016/j.bbrc.2024.150785. Epub 2024 Oct 2. PMID: 39369540.
2023
  1. Horii Y, Matsuda S, Toyota C, Morinaga T, Nakaya T, Tsuchiya S, Ohmuraya M, Hironaka T, Yoshiki R, Kasai K, Yamauchi Y, Takizawa N, Nagasaka A, Tanaka A, Kosako H, Nakaya M. VGLL3 is a mechanosensitive protein that promotes cardiac fibrosis through liquid-liquid phase separation. Nat Commun. 2023 Feb 8;14(1):550. doi: 10.1038/s41467-023-36189-6. PMID: 36754961; PMCID: PMC9908974.
  2. Hironaka T, Takizawa N, Yamauchi Y, Horii Y, Nakaya M. The well-developed actin cytoskeleton and Cthrc1 expression by actin-binding protein drebrin in myofibroblasts promote cardiac and hepatic fibrosis. J Biol Chem. 2023 Mar;299(3):102934. doi: 10.1016/j.jbc.2023.102934. Epub 2023 Jan 20. PMID: 36690273; PMCID: PMC9988570.
  3. Nagasaka A, Terawaki T, Noda M, Takashima M, Fujino M, Yamauchi Y, Arawaka S, Kato T, Nakaya M. GRK5-mediated inflammation and fibrosis exert cardioprotective effects during the acute phase of myocardial infarction. FEBS Open Bio. 2023 Feb;13(2):380-391. doi: 10.1002/2211-5463.13551. Epub 2023 Jan 20. PMID: 36633120; PMCID: PMC9900089.
  4. 末次春菜,吉岡啓佑，仲矢道雄「機械的刺激による筋線維芽細胞の性質変化」　生化学 95(3),1-4 (2023)
2021
  1. Takizawa N, Hironaka T, Mae K, Ueno T, Horii Y, Nagasaka A, Nakaya M. GPRC5B promotes collagen production in myofibroblasts. Biochem Biophys Res Commun. 2021 Jul 5;561:180-186. doi: 10.1016/j.bbrc.2021.05.035. Epub 2021 May 21. PMID: 34023784.
  2. Yoshida Y, Matsunaga N, Nakao T, Hamamura K, Kondo H, Ide T, Tsutsui H, Tsuruta A, Kurogi M, Nakaya M, Kurose H, Koyanagi S, Ohdo S. Alteration of circadian machinery in monocytes underlies chronic kidney disease-associated cardiac inflammation and fibrosis. Nat Commun. 2021 May 13;12(1):2783. doi: 10.1038/s41467-021-23050-x. PMID: 33986294; PMCID: PMC8119956.
2020
  1. Hironaka T, Ueno T, Mae K, Yoshimura C, Morinaga T, Horii Y, Nagasaka A, Kurose H, Nakaya M. Drebrin is induced during myofibroblast differentiation and enhances the production of fibrosis-related genes. Biochem Biophys Res Commun. 2020 Aug 20;529(2):224-230. doi: 10.1016/j.bbrc.2020.05.110. Epub 2020 Jun 22. PMID: 32703415.
  2. Horii Y, Nakaya M, Ohara H, Nishihara H, Watari K, Nagasaka A, Nakaya T, Sugiura Y, Okuno T, Koga T, Tanaka A, Yokomizo T, Kurose H. Leukotriene B4 receptor 1 exacerbates inflammation following myocardial infarction. FASEB J. 2020 Jun;34(6):8749-8763. doi: 10.1096/fj.202000041R. Epub 2020 May 8. PMID: 32385915.
  3. 仲矢道雄，堀井雄真，黒瀬等「死細胞貪食と線維化」　実験医学　増刊号「Fibrosis」Vol.38, No.12、88-93、(2020)

MESSAGE

We are committed to creating a research environment in which all lab members can enjoy their study and actively develop their careers.
We are currently recruiting postdoctoral researchers and graduate students. Please feel free to contact us for an informal inquiry.

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