Tao Liu
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Tao Liu has a total of 10 co-authors. Here are the top co-authors by number of shared publications:
- Deliang Liu
Department of Gastroenterology, Second Xiangya Hospital, Central South University, Changsha, China
2 shared publications - Jing Wu
Department of Gastroenterology, Second Xiangya Hospital, Central South University, Changsha 410011, China
2 shared publications - Liu Han
Department of Gastroenterology, Second Xiangya Hospital, Central South University, Changsha 410011, China
2 shared publications - Meihong Yu
Department of Gastroenterology, Second Xiangya Hospital, Central South University, Changsha 410011, China
2 shared publications - Yuyong Tan
Department of Gastroenterology, The Second Xiangya Hospital of Central South University, Changsha, Hunan, China
2 shared publications Haijun Deng
School of Mathematics & Statistics, Guizhou University of Finance and Economics, Guiyang 550025
1 shared publication
Latest Publications
- Open Access
- 24 June 2026
- Published by MDPI AG in Biomedicines
- Vol. 14 (7) , 1436
The Role of FGF1 in Chronic Liver Diseases
Chronic liver disease (CLD) constitutes a major global health burden, with high morbidity and mortality, limited treatment options for several etiologies, and an urgent need for novel therapeutic targets. Fibroblast growth factor 1 (FGF1) is a unique member of the FGF family capable of binding all four FGFR subtypes, thereby regulating multiple signaling pathways including PI3K/AKT, Ras/MAPK, and PLCγ, which are involved in metabolism, cell survival, proliferation, and tissue repair. Emerging evidence highlights the multifaceted and context-dependent roles of FGF1 in CLD. In drug-induced liver injury (DILI) caused by anti-tuberculosis drugs, acetaminophen, or doxorubicin, FGF1 confers protection by restoring bile acid homeostasis, reducing oxidative stress, inflammation, and apoptosis. In Metabolic dysfunction-associated steatotic liver disease (MASLD), FGF1 ameliorates hepatic steatosis, oxidative injury, and insulin resistance through downregulation of SREBP1, upregulation of PPARα, and activation of Nrf2-mediated antioxidant responses. Conversely, in primary sclerosing cholangitis (PSC), FGF1 aggravates ductular reaction, biliary senescence, and liver fibrosis via upregulation of SASP and TGF-β1, suggesting that inhibition of the FGF1/FGFR axis may be therapeutic. For alcohol-related liver disease (ALD), although direct experimental evidence is lacking, FGF1 is hypothesized to confer protection given its known activities against oxidative stress, lipid dysregulation, and cell death. Despite its promise, the mitogenic potential of FGF1 raises safety concerns; however, N-terminally modified FGF1 analogs (e.g., FGF1Δ) retain metabolic benefits with reduced proliferative activity. Collectively, FGF1 represents a versatile and disease-dependent regulator in CLD, warranting further mechanistic studies, safety evaluations, and development of targeted analogs as a novel therapeutic strategy for difficult-to-treat liver diseases.
- 24 June 2026
- Published by MDPI AG in Biomedicines
- Vol. 14 (7) , 1436
Open AccessThe Role of FGF1 in Chronic Liver Diseases
Chronic liver disease (CLD) constitutes a major global health burden, with high morbidity and mortality, limited treatment options for several etiologies, and an urgent need for novel therapeutic targets. Fibroblast growth factor 1 (FGF1) is a unique member of the FGF family capable of binding all four FGFR subtypes, thereby regulating multiple signaling pathways including PI3K/AKT, Ras/MAPK, and PLCγ, which are involved in metabolism, cell survival, proliferation, and tissue repair. Emerging evidence highlights the multifaceted and context-dependent roles of FGF1 in CLD. In drug-induced liver injury (DILI) caused by anti-tuberculosis drugs, acetaminophen, or doxorubicin, FGF1 confers protection by restoring bile acid homeostasis, reducing oxidative stress, inflammation, and apoptosis. In Metabolic dysfunction-associated steatotic liver disease (MASLD), FGF1 ameliorates hepatic steatosis, oxidative injury, and insulin resistance through downregulation of SREBP1, upregulation of PPARα, and activation of Nrf2-mediated antioxidant responses. Conversely, in primary sclerosing cholangitis (PSC), FGF1 aggravates ductular reaction, biliary senescence, and liver fibrosis via upregulation of SASP and TGF-β1, suggesting that inhibition of the FGF1/FGFR axis may be therapeutic. For alcohol-related liver disease (ALD), although direct experimental evidence is lacking, FGF1 is hypothesized to confer protection given its known activities against oxidative stress, lipid dysregulation, and cell death. Despite its promise, the mitogenic potential of FGF1 raises safety concerns; however, N-terminally modified FGF1 analogs (e.g., FGF1Δ) retain metabolic benefits with reduced proliferative activity. Collectively, FGF1 represents a versatile and disease-dependent regulator in CLD, warranting further mechanistic studies, safety evaluations, and development of targeted analogs as a novel therapeutic strategy for difficult-to-treat liver diseases.
- Open Access
- 21 May 2026
- Published by MDPI AG in Preprints.org
The Role of FGF1 in Chronic Liver Diseases
Chronic liver disease (CLD) constitutes a major global health burden, with high morbidity and mortality, limited treatment options for several etiologies, and an urgent need for novel therapeutic targets. Fibroblast growth factor 1 (FGF1) is a unique member of the FGF family capable of binding all four FGFR subtypes, thereby regulating multiple signaling pathways including PI3K/AKT, Ras/MAPK, and PLCγ, which are involved in metabolism, cell survival, proliferation, and tissue repair. Emerging evidence highlights the multifaceted and context-dependent roles of FGF1 in CLD. In drug-induced liver injury (DILI) caused by anti-tuberculosis drugs, acetaminophen, or doxorubicin, FGF1 exerts protective effects by restoring bile acid homeostasis, reducing oxidative stress, inflammation, and apoptosis. In metabolic-associated fatty liver disease (MAFLD), FGF1 ameliorates hepatic steatosis, oxidative injury, and insulin resistance through downregulation of SREBP1, upregulation of PPARα, and activation of Nrf2-mediated antioxidant responses. Conversely, in primary sclerosing cholangitis (PSC), FGF1 aggravates ductular reaction, biliary senescence, and liver fibrosis via upregulation of SASP and TGF-β1, suggesting that inhibition of the FGF1/FGFR axis may be therapeutic. For alcohol-related liver disease (ALD), although direct experimental evidence is lacking, FGF1 is hypothesized to confer protection given its known activities against oxidative stress, lipid dysregulation, and cell death. Despite its promise, the mitogenic potential of FGF1 raises safety concerns; however, N-terminally modified FGF1 analogs (e.g., FGF1Δ) retain metabolic benefits with reduced proliferative activity. Collectively, FGF1 represents a versatile and disease-dependent regulator in CLD, warranting further mechanistic studies, safety evaluations, and development of targeted analogs as a novel therapeutic strategy for difficult-to-treat liver diseases.
- 21 May 2026
- Published by MDPI AG in Preprints.org
Open AccessThe Role of FGF1 in Chronic Liver Diseases
Chronic liver disease (CLD) constitutes a major global health burden, with high morbidity and mortality, limited treatment options for several etiologies, and an urgent need for novel therapeutic targets. Fibroblast growth factor 1 (FGF1) is a unique member of the FGF family capable of binding all four FGFR subtypes, thereby regulating multiple signaling pathways including PI3K/AKT, Ras/MAPK, and PLCγ, which are involved in metabolism, cell survival, proliferation, and tissue repair. Emerging evidence highlights the multifaceted and context-dependent roles of FGF1 in CLD. In drug-induced liver injury (DILI) caused by anti-tuberculosis drugs, acetaminophen, or doxorubicin, FGF1 exerts protective effects by restoring bile acid homeostasis, reducing oxidative stress, inflammation, and apoptosis. In metabolic-associated fatty liver disease (MAFLD), FGF1 ameliorates hepatic steatosis, oxidative injury, and insulin resistance through downregulation of SREBP1, upregulation of PPARα, and activation of Nrf2-mediated antioxidant responses. Conversely, in primary sclerosing cholangitis (PSC), FGF1 aggravates ductular reaction, biliary senescence, and liver fibrosis via upregulation of SASP and TGF-β1, suggesting that inhibition of the FGF1/FGFR axis may be therapeutic. For alcohol-related liver disease (ALD), although direct experimental evidence is lacking, FGF1 is hypothesized to confer protection given its known activities against oxidative stress, lipid dysregulation, and cell death. Despite its promise, the mitogenic potential of FGF1 raises safety concerns; however, N-terminally modified FGF1 analogs (e.g., FGF1Δ) retain metabolic benefits with reduced proliferative activity. Collectively, FGF1 represents a versatile and disease-dependent regulator in CLD, warranting further mechanistic studies, safety evaluations, and development of targeted analogs as a novel therapeutic strategy for difficult-to-treat liver diseases.
- 28 June 2023
- Vol. 48 (6) , 859-867
消化内镜诊疗满意度量表的编制及评价
消化内镜在消化系统疾病诊疗中发挥重要作用。消化内镜诊疗满意度会直接影响患者的依从性,进而影响治疗效果。目前国内暂无评估消化内镜诊疗满意度的量表。本研究拟编制适合中国国情的消化内镜诊疗满意度量表,并评估其信效度,为临床评估消化内镜诊疗满意度提供工具。 通过查阅文献、访谈资深内镜医生和量表专家的方式编制消化内镜诊疗满意度原始量表。利用原始量表对120例患者进行第1轮调查,根据调查结果对原始量表进行分析、评价和修改,得到消化内镜诊疗满意度正式量表(以下简称“正式量表”);利用正式量表对另外200例患者进行第2轮调查,并根据调查结果对量表进行信度和效度的分析与评价。 原始量表信度良好但效度不佳。正式量表共有2个维度10个条目,克龙巴赫系数和分半信度系数分别为0.889和0.823,结构效度指标中,χ 2/df为2.513,近似误差均方根(root mean square error of approximation,RMSEA)为0.094,拟合优度指数(goodness of fit index,GFI)为0.914,调整后拟合优度指数(adjusted goodness of fit index,AGFI)为0.861,比较拟合指数(comparative fit index,CFI)为0.946,规范拟合指数(normed fit index,NFI)为0.915。聚合效度一般,区分效度良好,患者直接评分与量表总分具有较强的相关性。 消化内镜诊疗满意度量表具有良好的信效度,可以作为中国临床评估消化内镜诊疗满意度的工具。
- 28 June 2023
- Vol. 48 (6) , 859-867
消化内镜诊疗满意度量表的编制及评价
消化内镜在消化系统疾病诊疗中发挥重要作用。消化内镜诊疗满意度会直接影响患者的依从性,进而影响治疗效果。目前国内暂无评估消化内镜诊疗满意度的量表。本研究拟编制适合中国国情的消化内镜诊疗满意度量表,并评估其信效度,为临床评估消化内镜诊疗满意度提供工具。 通过查阅文献、访谈资深内镜医生和量表专家的方式编制消化内镜诊疗满意度原始量表。利用原始量表对120例患者进行第1轮调查,根据调查结果对原始量表进行分析、评价和修改,得到消化内镜诊疗满意度正式量表(以下简称“正式量表”);利用正式量表对另外200例患者进行第2轮调查,并根据调查结果对量表进行信度和效度的分析与评价。 原始量表信度良好但效度不佳。正式量表共有2个维度10个条目,克龙巴赫系数和分半信度系数分别为0.889和0.823,结构效度指标中,χ 2/df为2.513,近似误差均方根(root mean square error of approximation,RMSEA)为0.094,拟合优度指数(goodness of fit index,GFI)为0.914,调整后拟合优度指数(adjusted goodness of fit index,AGFI)为0.861,比较拟合指数(comparative fit index,CFI)为0.946,规范拟合指数(normed fit index,NFI)为0.915。聚合效度一般,区分效度良好,患者直接评分与量表总分具有较强的相关性。 消化内镜诊疗满意度量表具有良好的信效度,可以作为中国临床评估消化内镜诊疗满意度的工具。