Hongchi Jiang
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View article: Targeting complement C3 with Tanshinone I decreases microglia-mediated synaptic engulfment to exert antidepressant effects
Targeting complement C3 with Tanshinone I decreases microglia-mediated synaptic engulfment to exert antidepressant effects Open
Background: The limitations of current depression treatments highlight the importance of developing new therapeutic strategies. Tanshinone I (Tan I), a naturally occurring lipophilic diterpene compound, has promising activities including i…
View article: [Retracted] Hydroxytyrosol inhibits cholangiocarcinoma tumor growth: An in vivo and in vitro study
[Retracted] Hydroxytyrosol inhibits cholangiocarcinoma tumor growth: An in vivo and in vitro study Open
Following the publication of the above paper, a concerned reader drew to the Editor's attention that unexpected similarities existed among the β‑actin control western blots in Figs. 1B, 3E and 3G, albeit with the protein bands featured in …
View article: Identification of aging-related biomarkers for intervertebral disc degeneration in whole blood samples based on bioinformatics and machine learning
Identification of aging-related biomarkers for intervertebral disc degeneration in whole blood samples based on bioinformatics and machine learning Open
Introduction Aging is characterized by gradual structural and functional changes in the body over time, with intervertebral disc degeneration (IVDD) representing a key manifestation of spinal aging and a major contributor to low back pain …
View article: Arsenic trioxide preconditioning attenuates hepatic ischemia- reperfusion injury in mice: Role of ERK/AKT and autophagy
Arsenic trioxide preconditioning attenuates hepatic ischemia- reperfusion injury in mice: Role of ERK/AKT and autophagy Open
Background: Arsenic trioxide (ATO) is indicated as a broad-spectrum medicine for a variety of diseases, including cancer and cardiac disease. While the role of ATO in hepatic ischemia/reperfusion injury (HIRI) has not been reported. Thus, …
View article: Von Hippel-Lindau deficiency protects the liver against ischemia/reperfusion injury through the regulation of hypoxia-inducible factor 1α and 2α
Von Hippel-Lindau deficiency protects the liver against ischemia/reperfusion injury through the regulation of hypoxia-inducible factor 1α and 2α Open
Background: Ischemia and reperfusion (I/R)-induced liver injury contributes to morbidity and mortality during hepatic surgery or liver transplantation. As a pivotal regulator of cancer and inflammation, the role of Von Hippel-Lindau (VHL) …
View article: <scp>IRG1</scp> restrains <scp>M2</scp> macrophage polarization and suppresses intrahepatic cholangiocarcinoma progression via the <scp>CCL18</scp>/<scp>STAT3</scp> pathway
<span>IRG1</span> restrains <span>M2</span> macrophage polarization and suppresses intrahepatic cholangiocarcinoma progression via the <span>CCL18</span>/<span>STAT3</span> pathway Open
Intrahepatic cholangiocarcinoma (ICC) is a highly malignant and aggressive cancer whose incidence and mortality continue to increase, whereas its prognosis remains dismal. Tumor‐associated macrophages (TAMs) promote malignant progression a…
View article: TMEM147 aggravates the progression of HCC by modulating cholesterol homeostasis, suppressing ferroptosis, and promoting M2 polarization of TAMs
TMEM147 aggravates the progression of HCC by modulating cholesterol homeostasis, suppressing ferroptosis, and promoting M2 polarization of TAMs Open
Background: The endoplasmic reticulum (ER) regulates critical processes, including lipid synthesis, which can be affected by transmembrane proteins localized in the ER membrane. One of them, the transmembrane protein 147 (TMEM147) has been…
View article: Supplementary Figure 3 from Inhibition of Akt Reverses the Acquired Resistance to Sorafenib by Switching Protective Autophagy to Autophagic Cell Death in Hepatocellular Carcinoma
Supplementary Figure 3 from Inhibition of Akt Reverses the Acquired Resistance to Sorafenib by Switching Protective Autophagy to Autophagic Cell Death in Hepatocellular Carcinoma Open
PDF file - 166K, Supplementary Fig. S3. Sorafenib-resistant cells express different levels of p-Akt and autophagic proteins in vivo. Lysates of tumors harvested from (Fig. S1) at the end of experiments were subjected to immunoblotting.
View article: Supplementary Table 1 from Inhibition of Akt Reverses the Acquired Resistance to Sorafenib by Switching Protective Autophagy to Autophagic Cell Death in Hepatocellular Carcinoma
Supplementary Table 1 from Inhibition of Akt Reverses the Acquired Resistance to Sorafenib by Switching Protective Autophagy to Autophagic Cell Death in Hepatocellular Carcinoma Open
PDF file - 142K, Supplementary Table S1. Alteration of protein expression in sorafenib-resistant cells compared with parental cells in the presence or absence of sorafenib.
View article: Supplementary Figure 4 from Inhibition of Akt Reverses the Acquired Resistance to Sorafenib by Switching Protective Autophagy to Autophagic Cell Death in Hepatocellular Carcinoma
Supplementary Figure 4 from Inhibition of Akt Reverses the Acquired Resistance to Sorafenib by Switching Protective Autophagy to Autophagic Cell Death in Hepatocellular Carcinoma Open
PDF file - 327K, Supplementary Fig. S4.Akt inhibition or depletion synergizes with sorafenib to inhibit cell growth by regulating autophagic and apoptotic pathways in sorafenib-resistant HCC cells.
View article: Data from Inhibition of Akt Reverses the Acquired Resistance to Sorafenib by Switching Protective Autophagy to Autophagic Cell Death in Hepatocellular Carcinoma
Data from Inhibition of Akt Reverses the Acquired Resistance to Sorafenib by Switching Protective Autophagy to Autophagic Cell Death in Hepatocellular Carcinoma Open
Sorafenib is the standard first-line systemic drug for advanced hepatocellular carcinoma (HCC), but the acquired resistance to sorafenib results in limited benefits. Activation of Akt is thought to be responsible for mediating the acquired…
View article: Supplementary Figure 1 from Inhibition of Akt Reverses the Acquired Resistance to Sorafenib by Switching Protective Autophagy to Autophagic Cell Death in Hepatocellular Carcinoma
Supplementary Figure 1 from Inhibition of Akt Reverses the Acquired Resistance to Sorafenib by Switching Protective Autophagy to Autophagic Cell Death in Hepatocellular Carcinoma Open
PDF file - 109K, Supplementary Fig. S 1. Sorafenib-resistant cells responded poorly to sorafenib treatment in vivo.Parental Huh7 and Huh7-SR tumors were established in mice, which received different treatments for 15 days and then euthaniz…
View article: Supplementary Table 1 from Inhibition of Akt Reverses the Acquired Resistance to Sorafenib by Switching Protective Autophagy to Autophagic Cell Death in Hepatocellular Carcinoma
Supplementary Table 1 from Inhibition of Akt Reverses the Acquired Resistance to Sorafenib by Switching Protective Autophagy to Autophagic Cell Death in Hepatocellular Carcinoma Open
PDF file - 142K, Supplementary Table S1. Alteration of protein expression in sorafenib-resistant cells compared with parental cells in the presence or absence of sorafenib.
View article: Supplementary Figure 5 from Inhibition of Akt Reverses the Acquired Resistance to Sorafenib by Switching Protective Autophagy to Autophagic Cell Death in Hepatocellular Carcinoma
Supplementary Figure 5 from Inhibition of Akt Reverses the Acquired Resistance to Sorafenib by Switching Protective Autophagy to Autophagic Cell Death in Hepatocellular Carcinoma Open
PDF file - 225K, Supplementary Fig. S5.Interactions of Akt, autophagic and apoptotic pathways in sorafenib-resistant HCC cells.(A) Immunoblots of lysates of HepG2-SR and Huh7-SR cells following incubation with sorafenib (10 μM), GDC0068 (5…
View article: Supplementary Figure 5 from Inhibition of Akt Reverses the Acquired Resistance to Sorafenib by Switching Protective Autophagy to Autophagic Cell Death in Hepatocellular Carcinoma
Supplementary Figure 5 from Inhibition of Akt Reverses the Acquired Resistance to Sorafenib by Switching Protective Autophagy to Autophagic Cell Death in Hepatocellular Carcinoma Open
PDF file - 225K, Supplementary Fig. S5.Interactions of Akt, autophagic and apoptotic pathways in sorafenib-resistant HCC cells.(A) Immunoblots of lysates of HepG2-SR and Huh7-SR cells following incubation with sorafenib (10 μM), GDC0068 (5…
View article: Data from Inhibition of Akt Reverses the Acquired Resistance to Sorafenib by Switching Protective Autophagy to Autophagic Cell Death in Hepatocellular Carcinoma
Data from Inhibition of Akt Reverses the Acquired Resistance to Sorafenib by Switching Protective Autophagy to Autophagic Cell Death in Hepatocellular Carcinoma Open
Sorafenib is the standard first-line systemic drug for advanced hepatocellular carcinoma (HCC), but the acquired resistance to sorafenib results in limited benefits. Activation of Akt is thought to be responsible for mediating the acquired…
View article: Supplementary Figure 2 from Inhibition of Akt Reverses the Acquired Resistance to Sorafenib by Switching Protective Autophagy to Autophagic Cell Death in Hepatocellular Carcinoma
Supplementary Figure 2 from Inhibition of Akt Reverses the Acquired Resistance to Sorafenib by Switching Protective Autophagy to Autophagic Cell Death in Hepatocellular Carcinoma Open
PDF file - 224K, Supplementary Fig. S2.Sorafenib activates the Akt pathway independent of PP2A in hepatocellular carcinoma cells.
View article: Supplementary Figure 1 from Inhibition of Akt Reverses the Acquired Resistance to Sorafenib by Switching Protective Autophagy to Autophagic Cell Death in Hepatocellular Carcinoma
Supplementary Figure 1 from Inhibition of Akt Reverses the Acquired Resistance to Sorafenib by Switching Protective Autophagy to Autophagic Cell Death in Hepatocellular Carcinoma Open
PDF file - 109K, Supplementary Fig. S 1. Sorafenib-resistant cells responded poorly to sorafenib treatment in vivo.Parental Huh7 and Huh7-SR tumors were established in mice, which received different treatments for 15 days and then euthaniz…
View article: Supplementary Figure 3 from Inhibition of Akt Reverses the Acquired Resistance to Sorafenib by Switching Protective Autophagy to Autophagic Cell Death in Hepatocellular Carcinoma
Supplementary Figure 3 from Inhibition of Akt Reverses the Acquired Resistance to Sorafenib by Switching Protective Autophagy to Autophagic Cell Death in Hepatocellular Carcinoma Open
PDF file - 166K, Supplementary Fig. S3. Sorafenib-resistant cells express different levels of p-Akt and autophagic proteins in vivo. Lysates of tumors harvested from (Fig. S1) at the end of experiments were subjected to immunoblotting.
View article: Supplementary Figure 4 from Inhibition of Akt Reverses the Acquired Resistance to Sorafenib by Switching Protective Autophagy to Autophagic Cell Death in Hepatocellular Carcinoma
Supplementary Figure 4 from Inhibition of Akt Reverses the Acquired Resistance to Sorafenib by Switching Protective Autophagy to Autophagic Cell Death in Hepatocellular Carcinoma Open
PDF file - 327K, Supplementary Fig. S4.Akt inhibition or depletion synergizes with sorafenib to inhibit cell growth by regulating autophagic and apoptotic pathways in sorafenib-resistant HCC cells.
View article: Supplementary Figure 2 from Inhibition of Akt Reverses the Acquired Resistance to Sorafenib by Switching Protective Autophagy to Autophagic Cell Death in Hepatocellular Carcinoma
Supplementary Figure 2 from Inhibition of Akt Reverses the Acquired Resistance to Sorafenib by Switching Protective Autophagy to Autophagic Cell Death in Hepatocellular Carcinoma Open
PDF file - 224K, Supplementary Fig. S2.Sorafenib activates the Akt pathway independent of PP2A in hepatocellular carcinoma cells.
View article: [Variables associated with hematological remission and survival in patients with acute myeloid leukemia after induction failure and relapse].
[Variables associated with hematological remission and survival in patients with acute myeloid leukemia after induction failure and relapse]. Open
Objective: This study aimed to explore variables associated with remission rate and survival in patients with acute myeloid leukemia (AML) after induction failure and relapse. Methods: Data of 373 consecutive patients with AML were analyze…
View article: Integrative Analysis of the Roles of lncRNAs and mRNAs in Itaconate-Mediated Protection Against Liver Ischemia-Reperfusion Injury in Mice
Integrative Analysis of the Roles of lncRNAs and mRNAs in Itaconate-Mediated Protection Against Liver Ischemia-Reperfusion Injury in Mice Open
Our study revealed that itaconate could protect the liver against IR injury and that lncRNAs might play a role in this process. Our study provides a novel way to investigate the mechanism by which itaconate affects hepatic IR injury and ex…