Article
Cell Biology
Hiroyuki Ogawa, Kosuke Kaji, Norihisa Nishimura, Hirotetsu Takagi, Koji Ishida, Hiroaki Takaya, Hideto Kawaratani, Kei Moriya, Tadashi Namisaki, Takemi Akahane, Hitoshi Yoshiji
Summary: Lenvatinib shows potential as a novel therapeutic strategy for liver fibrosis by inhibiting hepatic stellate cell proliferation and promoting apoptosis, as well as reducing protein expression levels and intrahepatic neovascularization.
JOURNAL OF CELLULAR AND MOLECULAR MEDICINE
(2021)
Article
Fisheries
Quanquan Cao, Hongying Shan, Ju Zhao, Jinhe Deng, Man Xu, Hao Kang, Tong Li, Ye Zhao, Haifeng Liu, Jun Jiang
Summary: Liver fibrosis is a pathological process characterized by the activation of hepatic stellate cells, imbalance of extracellular matrix generation, and deposition in the liver. This review focuses on the understanding of liver fibrosis in aquaculture fish, discussing its pathophysiology, diagnosis methods, and treatment options. The article highlights the importance of further research in order to develop effective prevention and treatment strategies for liver fibrosis in fish, ensuring the sustainability of aquaculture and the health of farmed fish.
FISH & SHELLFISH IMMUNOLOGY
(2023)
Review
Biochemistry & Molecular Biology
Yufei Yan, Jiefei Zeng, Linhao Xing, Changyong Li
Summary: Hepatic fibrosis is characterized by the accumulation of extracellular matrix in the liver due to persistent injury. Understanding the cellular and molecular mechanisms controlling the fibrotic response is crucial for developing clinical strategies to prevent fibrosis progression. Activation of hepatic stellate cells plays a key role in promoting ECM synthesis, and various external signals contribute to this process.
Article
Immunology
Jie Wang, Lina Yang, Jialing You, Dada Wen, Bo Yang, Canhua Jiang
Summary: The study found that PDGF-BB can induce autophagy of oral mucosal fibroblasts through the interaction of Beclin-1 and PI3KC3, promoting cell proliferation, migration, and collagen synthesis. However, the inhibition of this interaction weakened the fibroblasts' activities. Overall, PDGF-BB regulates the biological behavior of oral mucosal fibroblasts by inducing autophagy through the Beclin-1 pathway.
JOURNAL OF INFLAMMATION RESEARCH
(2021)
Article
Biochemistry & Molecular Biology
Sam Seok Cho, Ji Hye Yang, Ji Hyun Lee, Jin Sol Baek, Sae Kwang Ku, Il Je Cho, Kyu Min Kim, Sung Hwan Ki
Summary: The study suggests that ferroptosis contributes to the progression of hepatic fibrosis by activating hepatic stellate cells and increasing the expression of fibrosis markers.
FREE RADICAL BIOLOGY AND MEDICINE
(2022)
Article
Biochemistry & Molecular Biology
Floris Haijer, Shiva Koets-Shajari, Janette Heegsma, Sandra Serna-Salas, Tjasso Blokzijl, Manon Buist-Homan, Han Moshage, Klaas Nico Faber
Summary: Liver fibrosis is caused by excessive proliferation and collagen production by hepatic stellate cells (HSCs) due to chronic liver injury. Hydroxyurea, an anti-proliferative drug, showed inhibitory effects on HSC proliferation and fibrosis development in both in vitro and in vivo experiments. This study provides evidence for the therapeutic potential of hydroxyurea in treating liver fibrosis.
Article
Cell Biology
Yiming Zhu, Chihao Zhang, Mingzhe Huang, Jiayun Lin, Xiao Fan, Tao Ni
Summary: In this study, the researchers found that TRIM26 promotes HSCs ferroptosis through mediating the ubiquitination of SLC7A11, thereby suppressing liver fibrosis. The targeted suppression of SLC7A11 by TRIM26 could be a novel therapeutic strategy for liver fibrosis.
FRONTIERS IN CELL AND DEVELOPMENTAL BIOLOGY
(2021)
Article
Plant Sciences
Ke Chen, Weiran Guo, Rongxin Li, Yueqing Han, Qi Gao, Shuzhen Wang
Summary: This study investigates the antifibrotic properties of T-96 and its underlying molecular mechanisms. The results show that T-96 can inhibit the proliferation, migration, and activation of hepatic stellate cells and alleviate liver injury, inflammation, and fibrosis progression in a CCl4-induced liver fibrosis mouse model. Mechanistic studies reveal that the antifibrotic effect of T-96 is mediated by suppressing the expression of AGAP2 and inhibiting the phosphorylation of FAK and AKT.
Review
Gastroenterology & Hepatology
Leke Wiering, Pallavi Subramanian, Linda Hammerich
Summary: Nonalcoholic fatty liver disease (NAFLD) is a common chronic liver disease with a wide range of severity, from simple hepatic steatosis to nonalcoholic steatohepatitis (NASH). NASH can lead to liver fibrosis, cirrhosis, and hepatocellular carcinoma, making hepatic fibrosis an important predictor of outcomes. Recent advancements in understanding the activation and inactivation of hepatic stellate cells, which drive fibrosis development, have shed light on the disease progression in NAFLD/NASH.
CELLULAR AND MOLECULAR GASTROENTEROLOGY AND HEPATOLOGY
(2023)
Article
Biochemistry & Molecular Biology
Hanglu Ying, Long Li, Yufen Zhao, Feng Ni
Summary: This study evaluated the function of ivermectin in regulating liver fibrosis. The results showed that ivermectin alleviated histopathological changes, improved liver function, reduced collagen deposition, and downregulated the expression of profibrotic genes. Mechanistically, it inhibited intrahepatic macrophage accumulation and suppressed the production of proinflammatory factors. Importantly, it also promoted HSC deactivation by reducing the protein levels of alpha-smooth muscle actin (alpha-SMA).
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2022)
Article
Cell Biology
Xiaoyan Chen, Wenjie Shi, Liang Zhu, Xiaojiang Zhou, Yunwu Wang
Summary: Liver fibrosis is caused by the activation of hepatic stellate cells (HSCs) due to chronic liver damage. This study investigates the protective role of CFIm25 in inhibiting HSC activation and its underlying mechanisms. CFIm25 expression was found to be decreased in activated murine HSCs and fibrotic liver tissues. CFIm25 overexpression down-regulated fibrosis-related genes, inhibiting HSC activation, migration, and proliferation through the KLF14/PPARγ signaling axis. These findings suggest that CFIm25 may be a potential therapeutic target for liver fibrosis.
CELLULAR SIGNALLING
(2023)
Article
Chemistry, Medicinal
Guofang Liu, Can Wei, Siyu Yuan, Zhe Zhang, Jiahao Li, Lijun Zhang, Guokai Wang, Ling Fang
Summary: This study found that Wogonoside (WG) alleviates liver fibrosis by inducing ferroptosis in hepatic stellate cells (HSCs), providing a new clue for the treatment of liver fibrosis.
PHYTOTHERAPY RESEARCH
(2022)
Review
Endocrinology & Metabolism
James K. Carter, Scott L. Friedman
Summary: Nonalcoholic fatty liver disease (NAFLD) is the main cause of liver disease worldwide, and nonalcoholic steatohepatitis (NASH) is a more severe form characterized by significant hepatocellular injury, inflammation, and fibrosis. Recent research has shown that heightened immune cell activity and chronic inflammation play crucial roles in the development of NASH, with hepatic stellate cells (HSCs) being the key drivers of fibrosis.
FRONTIERS IN ENDOCRINOLOGY
(2022)
Article
Immunology
Fangbin Liu, Shengnan Li, Panpan Chen, Yanqiu Gu, Shaozhan Wang, Lei Wang, Chun Chen, Rong Wang, Yongfang Yuan
Summary: Liver fibrosis is a reversible pathological process that can lead to liver failure and cancer. Salvia miltiorrhiza is a medicinal plant with hepatoprotective effects, and its component Salvianolic acid B has been found to have anti-liver fibrosis effects. This study discovered that Sal B targets PDGFR beta to inhibit the activation, migration, and proliferation of hepatic stellate cells, which are closely related to liver fibrosis.
INTERNATIONAL IMMUNOPHARMACOLOGY
(2023)
Article
Nutrition & Dietetics
Shimon Reif, Ariel Atias, Mirit Musseri, Nickolay Koroukhov, Regina Golan Gerstl
Summary: This study investigated whether milk-derived extracellular vesicles (MDEs) can regulate the progression of liver fibrosis by inhibiting the activation of hepatic stellate cells (HSCs). The results showed that MDEs can enter HSCs in vitro and in vivo, inhibiting their proliferation and regulating their activation.
Article
Oncology
U. Toh, N. Iwakuma, M. Mishima, M. Okabe, S. Nakagawa, Y. Akagi
BREAST CANCER RESEARCH AND TREATMENT
(2015)
Article
Oncology
Shinjiro Sakamoto, Satoko Matsueda, Shinzo Takamori, Uhi Toh, Masanori Noguchi, Shigeru Yutani, Akira Yamada, Shigeki Shichijo, Teppei Yamada, Shigetaka Suekane, Kouichiro Kawano, Tetsuro Sasada, Noboru Hattori, Nobuoki Kohno, Kyogo Itoh
Article
Oncology
Tomohiro Shibata, Kosuke Watari, Hiroto Izumi, Akihiko Kawahara, Satoshi Hattori, Chihiro Fukumitsu, Yuichi Murakami, Ryuji Takahashi, Uhi Toh, Ken-ichi Ito, Shigehiro Ohdo, Maki Tanaka, Masayoshi Kage, Michihiko Kuwano, Mayumi Ono
Article
Oncology
Reiki Nishimura, Uhi Toh, Maki Tanaka, Michiyo Saimura, Yasuhiro Okumura, Tsuyoshi Saito, Toshihiro Tanaka, Megumi Teraoka, Kazuo Shimada, Kazuhisa Katayama, Toshihiro Koga, Kaname Kurashita, Satoshi Hasegawa, Hidekazu Todoroki, Yuichiro Kai, Yasuyo Ohi, Satoshi Toyoshima, Nobuyuki Arima, Shoshu Mitsuyama, Kazuo Tamura
Article
Oncology
Mari S. Oba, Shigeru Imoto, Uhi Toh, Noriaki Wada, Masaya Kawada, Masahiro Kitada, Norikazu Masuda, Tetsuya Taguchi, Shigeki Minami, Hiromitsu Jinno, Junichi Sakamoto, Satoshi Morita
JAPANESE JOURNAL OF CLINICAL ONCOLOGY
(2014)
Article
Surgery
Daisuke Muroya, Uhi Toh, Nobutaka Iwakuma, Shino Nakagawa, Mai Mishima, Ryuji Takahashi, Miki Takenaka, Kazuo Shirouzu, Yoshito Agaki
Article
Oncology
Hiroko Otsuka, Teruhiko Fujii, Uhi Toh, Nobutaka Iwakuma, Ryuji Takahashi, Mai Mishima, Miki Takenaka, Tatsuyuki Kakuma, Maki Tanaka, Kazuo Shirouzu
Article
Oncology
Mai Mishima, Uhi Toh, Nobutaka Iwakuma, Miki Takenaka, Mina Furukawa, Yoshito Akagi
Article
Cell Biology
Momoko Akashi, Rin Yamaguchi, Hironori Kusano, Hitoshi Obara, Miki Yamaguchi, Uhi Toh, Jun Akiba, Tatsuyuki Kakuma, Maki Tanaka, Yoshito Akagi, Hirohisa Yano
Article
Oncology
Uhi Toh, Sayaka Sakurai, Shuko Saku, Yuko Takao, Mina Okabe, Nobutaka Iwakuma, Shigeki Shichijo, Akira Yamada, Kyogo Itoh, Yoshito Akagi
Article
Radiology, Nuclear Medicine & Medical Imaging
Hayato Kaida, Koichi Azuma, Uhi Toh, Akihiko Kawahara, Eiji Sadashima, Satoshi Hattori, Jun Akiba, Nobuhiro Tahara, Axel Rominger, Kazunari Ishii, Takamichi Murakami, Masatoshi Ishibashi
HELLENIC JOURNAL OF NUCLEAR MEDICINE
(2018)
Article
Oncology
Mina Okabe, Uhi Toh, Nobutaka Iwakuma, Shuko Saku, Momoko Akashi, Yuko Kimitsuki, Naoko Seki, Akihiko Kawahara, Etsuyo Ogo, Kyogo Itoh, Yoshito Akagi
Article
Oncology
Shinjiro Sakamoto, Satoko Matsueda, Shinzo Takamori, Uhi Toh, Masanori Noguchi, Shigeru Yutani, Akira Yamada, Shigeki Shichijo, Teppei Yamada, Shigetaka Suekane, Kouichiro Kawano, Masayasu Naitou, Tetsuro Sasada, Noboru Hattori, Nobuoki Kohno, Kyogo Itoh
Article
Oncology
Ryuji Takahashi, Uhi Toh, Nobutaka Iwakuma, Miki Takenaka, Hiroko Otsuka, Mina Furukawa, Teruhiko Fujii, Naoko Seki, Akihiko Kawahara, Masayoshi Kage, Satoko Matsueda, Yoshito Akagi, Akira Yamada, Kyogo Itoh, Tetsuro Sasada
BREAST CANCER RESEARCH
(2014)
Article
Oncology
Teruhiko Fujii, Keisuke Miwa, Tomoyuki Ushijima, Mototsugu Matsunaga, Masaru Fukahori, Kotaro Yuge, Uhi Toh, Nobutaka Iwakuma, Ryuji Takahashi, Hiroki Takahashi, Miki Takenaka, Mai Mishima, Yoshito Akagi, Masayoshi Kage, Shino Nakagawa
CURRENT CANCER THERAPY REVIEWS
(2014)