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Article ; Online: Platelets in Renal Disease.

Gomchok, Drolma / Ge, Ri-Li / Wuren, Tana

International journal of molecular sciences

2023 Volume 24, Issue 19

Abstract: Kidney disease is a major global health concern, affecting millions of people. Nephrologists have shown interest in platelets because of coagulation disorders caused by renal diseases. With a better understanding of platelets, it has been found that ... ...

Abstract	Kidney disease is a major global health concern, affecting millions of people. Nephrologists have shown interest in platelets because of coagulation disorders caused by renal diseases. With a better understanding of platelets, it has been found that these anucleate and abundant blood cells not only play a role in hemostasis, but also have important functions in inflammation and immunity. Platelets are not only affected by kidney disease, but may also contribute to kidney disease progression by mediating inflammation and immune effects. This review summarizes the current evidence regarding platelet abnormalities in renal disease, and the multiple effects of platelets on kidney disease progression. The relationship between platelets and kidney disease is still being explored, and further research can provide mechanistic insights into the relationship between thrombosis, bleeding, and inflammation related to kidney disease, and elucidate targeted therapies for patients with kidney disease.
MeSH term(s)	Humans ; Immunity, Innate ; Blood Platelets ; Hemostasis ; Inflammation ; Kidney Diseases/complications ; Disease Progression
Language	English
Publishing date	2023-09-29
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms241914724
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: [Research progress on the effect of mitochondrial and endoplasmic reticulum stress caused by hypoxia during pregnancy on preeclampsia and intrauterine growth restriction].

Liu, Hui-Fang / Ge, Ri-Li / Wuren, Ta-Na

Sheng li xue bao : [Acta physiologica Sinica

2023 Volume 75, Issue 5, Page(s) 714–726

Abstract: Preeclampsia and intrauterine growth restriction (IUGR) of the fetus are the two most common pregnancy complications worldwide, affecting 5%-10% of pregnant women. Preeclampsia is associated with significantly increased maternal and fetal morbidity and ... ...

Abstract	Preeclampsia and intrauterine growth restriction (IUGR) of the fetus are the two most common pregnancy complications worldwide, affecting 5%-10% of pregnant women. Preeclampsia is associated with significantly increased maternal and fetal morbidity and mortality. Hypoxia-induced uteroplacental dysfunction is now recognized as a key pathological factor in preeclampsia and IUGR. Reduced oxygen supply (hypoxia) disrupts mitochondrial and endoplasmic reticulum (ER) function. Hypoxia has been shown to alter mitochondrial reactive oxygen species (ROS) homeostasis and induce ER stress. Hypoxia during pregnancy is associated with excessive production of ROS in the placenta, leading to oxidative stress. Oxidative stress occurs in a number of human diseases, including high blood pressure during pregnancy. Studies have shown that uterine placental tissue/cells in preeclampsia and IUGR show high levels of oxidative stress, which plays an important role in the pathogenesis of both the complications. This review summarizes the role of hypoxia-induced mitochondrial oxidative stress and ER stress in the pathogenesis of preeclampsia/IUGR and discusses the potential therapeutic strategies targeting oxidative stress to treat both the pregnancy complications.
MeSH term(s)	Pregnancy ; Female ; Humans ; Placenta ; Fetal Growth Retardation/etiology ; Pre-Eclampsia/etiology ; Pre-Eclampsia/pathology ; Reactive Oxygen Species ; Hypoxia/pathology ; Pregnancy Complications/pathology ; Endoplasmic Reticulum Stress
Chemical Substances	Reactive Oxygen Species
Language	Chinese
Publishing date	2023-11-02
Publishing country	China
Document type	Review ; English Abstract ; Journal Article
ZDB-ID	604308-2
ISSN	0371-0874
ISSN	0371-0874
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Zs.A 386: Show issues

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Article: Hypoxia-inducible factor-2α promotes fibrosis in non-alcoholic fatty liver disease by enhancing glutamine catabolism and inhibiting yes-associated protein phosphorylation in hepatic stellate cells.

Yan, Ranran / Cai, Hao / Zhou, Xiaofeng / Bao, Guodan / Bai, Zhenzhong / Ge, Ri-Li

Frontiers in endocrinology

2024 Volume 15, Page(s) 1344971

Abstract: Non-alcoholic fatty liver disease (NAFLD) has a high global prevalence and affects approximately one-third of adults, owing to high-fat dietary habits and a sedentary lifestyle. The role of hypoxia-inducible factor 2α (HIF-2α) in NAFLD progression ... ...

Abstract	Non-alcoholic fatty liver disease (NAFLD) has a high global prevalence and affects approximately one-third of adults, owing to high-fat dietary habits and a sedentary lifestyle. The role of hypoxia-inducible factor 2α (HIF-2α) in NAFLD progression remains unknown. This study aimed to investigate the effects of chronic hypoxia on NAFLD progression by examining the role of hypoxia-inducible factor 2α (HIF-2α) activation and that of hepatic stellate cell (HSC)-derived myofibroblasts through glutaminolysis. We hypothesised that hypoxia exacerbates NAFLD by promoting HIF-2α upregulation and inhibiting phosphorylated yes-associated protein (YAP), and that increasing YAP expression enhances HSC-derived myofibroblasts. We studied patients with NAFLD living at high altitudes, as well as animal models and cultured cells. The results revealed significant increases in HSC-derived myofibroblasts and collagen accumulation caused by HIF-2α and YAP upregulation, both in patients and in a mouse model for hypoxia and NAFLD. HIF-2α and HIF-2α-dependent YAP downregulation reduced HSC activation and myofibroblast levels in persistent chronic hypoxia. Furthermore, hypoxia-induced HIF-2α upregulation promoted YAP and inhibited YAP phosphorylation, leading to glutaminase 1 (GLS1), SLC38A1, α-SMA, and Collagen-1 overexpression. Additionally, hypoxia restored mitochondrial adenosine triphosphate production and reactive oxygen species (ROS) overproduction. Thus, chronic hypoxia-induced HIF-2α activation enhances fibrosis and NAFLD progression by restoring mitochondrial ROS production and glutaminase-1-induced glutaminolysis, which is mediated through the inhibition of YAP phosphorylation and increased YAP nuclear translocation. In summary, HIF-2α plays a pivotal role in NAFLD progression during chronic hypoxia.
MeSH term(s)	Adult ; Animals ; Humans ; Mice ; Basic Helix-Loop-Helix Transcription Factors/metabolism ; Collagen Type I/metabolism ; Glutaminase/metabolism ; Glutamine/metabolism ; Hepatic Stellate Cells/metabolism ; Hypoxia/metabolism ; Liver Cirrhosis/metabolism ; Non-alcoholic Fatty Liver Disease/metabolism ; Phosphorylation ; Reactive Oxygen Species/metabolism ; YAP-Signaling Proteins
Chemical Substances	Basic Helix-Loop-Helix Transcription Factors ; Collagen Type I ; Glutaminase (EC 3.5.1.2) ; Glutamine (0RH81L854J) ; Reactive Oxygen Species ; YAP-Signaling Proteins ; Yap1 protein, mouse ; YAP1 protein, human ; endothelial PAS domain-containing protein 1 (1B37H0967P)
Language	English
Publishing date	2024-02-28
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2592084-4
ISSN	1664-2392
ISSN	1664-2392
DOI	10.3389/fendo.2024.1344971
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Article: [Effects of human umbilical cord mesenchymal stem cells (MSCs)-derived exosomes on pulmonary vascular remodeling in hypoxic pulmonary hypertension].

Liu, Hong / Zhang, Yu-Wei / Zhang, Qing-Qing / Wang, Yu-Xiang / Ge, Ri-Li / Ma, Lan

Sheng li xue bao : [Acta physiologica Sinica

2024 Volume 76, Issue 1, Page(s) 33–44

Abstract: The present study aimed to investigate the effect of human umbilical cord mesenchymal stem cells (MSCs)-derived exosomes (MSCs-Exo) on mice with hypoxic pulmonary hypertension (HPH). MSCs were isolated and cultured from human umbilical cords under ... ...

Abstract	The present study aimed to investigate the effect of human umbilical cord mesenchymal stem cells (MSCs)-derived exosomes (MSCs-Exo) on mice with hypoxic pulmonary hypertension (HPH). MSCs were isolated and cultured from human umbilical cords under aseptic conditions, and exosomes were extracted from the supernatants and identified. Healthy SPF C57BL/6 mice were randomly divided into three groups: normoxic group, hypoxic group, and hypoxic+MSCs-Exo group. Mice in the hypoxic group and the hypoxic+MSCs-Exo group were maintained for 28 d at an equivalent altitude of 5 000 m in a hypobaric chamber to establish HPH mouse model. The mice in the hypoxic+MSCs-Exo group were injected with MSCs-Exo via tail vein before hypoxia and on days 1, 3, 5 and 9 of hypoxia, and the mice in the other two groups were injected with PBS. At the end of the experiment, echocardiography was performed to detect pulmonary arterial acceleration time/pulmonary arterial ejection time ratio (PAAT/PET), right ventricular free wall thickness, and right ventricular hypertrophy index RV/(LV+S). HE staining was performed to observe the lung tissue morphology. EVG staining was performed to observe elastic fiber hyperplasia. Immunohistochemistry was performed to detect α smooth muscle actin (α-SMA) expression in lung tissue. Immunofluorescence staining was used to detect macrophage infiltration in lung tissue. qPCR was performed to detect IL-1β and IL-33 in lung tissue, and cytometric bead array was performed to detect IL-10 secretion. Western blotting was used to detect the M1 macrophage marker iNOS, M2 macrophage marker Arg-1 and IL-33/ST2 pathway proteins in lung tissues. The results showed that hypoxia increased pulmonary artery pressure and pulmonary vascular remodeling, increased macrophage infiltration, IL-1β and IL-33 expression (P < 0.05) and upregulated the IL-33/ST2 pathway (P < 0.05). Compared with the hypoxic group, MSCs-Exo treatment increased PAAT/PET (P < 0.05), decreased right ventricular free wall thickness (P < 0.05), right ventricular hypertrophy index RV/(LV+S) (P < 0.05), α-SMA expression in small pulmonary vessels (P < 0.05), and inflammatory factors including IL-1β and IL-33 expression in lung tissue, however increased IL-10 secretion (P < 0.05). In addition, MSCs-Exo treatment upregulated Arg-1 and downregulated iNOS and IL-33/ST2 (P < 0.05). The results suggest that MSC-Exo may alleviate HPH through their immunomodulatory effects.
MeSH term(s)	Humans ; Animals ; Mice ; Mice, Inbred C57BL ; Hypertension, Pulmonary ; Interleukin-10 ; Interleukin-33 ; Exosomes ; Hypertrophy, Right Ventricular ; Interleukin-1 Receptor-Like 1 Protein ; Vascular Remodeling ; Hypoxia ; Mesenchymal Stem Cells ; Lung
Chemical Substances	Interleukin-10 (130068-27-8) ; Interleukin-33 ; Interleukin-1 Receptor-Like 1 Protein
Language	Chinese
Publishing date	2024-02-28
Publishing country	China
Document type	English Abstract ; Journal Article
ZDB-ID	604308-2
ISSN	0371-0874
ISSN	0371-0874
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Zs.A 386: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (1.OG)
ab Jg. 2022: Lesesaal (EG)

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Article: Ubenimex combined with Albendazole for the treatment of

Zhou, Zhen / Huayu, Meiduo / Mu, Yalin / Tang, Feng / Ge, Ri-Li

Frontiers in veterinary science

2024 Volume 11, Page(s) 1320308

Abstract: Introduction: Alveolar echinococcosis (AE) is a parasitic disease caused by : Methods: In this study, the therapeutic effect of Ubenimex combined with Albendazole on AE was evaluated. Mice were intraperitoneally injected with : Results: The ... ...

Abstract	Introduction: Alveolar echinococcosis (AE) is a parasitic disease caused by Methods: In this study, the therapeutic effect of Ubenimex combined with Albendazole on AE was evaluated. Mice were intraperitoneally injected with Results: The results revealed that the combined treatment could inhibit the growth and infiltration of cysts in BALB/c mice infected with Discussion: This study suggests that the combined treatment with Ubenimex and Albendazole could be a potential therapeutic strategy for
Language	English
Publishing date	2024-03-15
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2834243-4
ISSN	2297-1769
ISSN	2297-1769
DOI	10.3389/fvets.2024.1320308
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Article: High-Altitude Hypoxia Induces Excessive Erythrocytosis in Mice via Upregulation of the Intestinal

Zhou, Sisi / Yan, Jun / Song, Kang / Ge, Ri-Li

Biomedicines

2023 Volume 11, Issue 11

Abstract: Excessive erythrocytosis (EE) is a preclinical form of chronic mountain sickness (CMS). The dysregulation of iron metabolism in high-altitude hypoxia may induce EE. The intestinal hypoxia-inducible factor 2 alpha ( ...

Abstract	Excessive erythrocytosis (EE) is a preclinical form of chronic mountain sickness (CMS). The dysregulation of iron metabolism in high-altitude hypoxia may induce EE. The intestinal hypoxia-inducible factor 2 alpha (
Language	English
Publishing date	2023-11-07
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2720867-9
ISSN	2227-9059
ISSN	2227-9059
DOI	10.3390/biomedicines11112992
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Article: [Factors affecting pulmonary arterial pressure in response to high-altitude hypoxic stress].

Zhou, Zhen / Tang, Feng / Ge, Ri-Li

Sheng li xue bao : [Acta physiologica Sinica

2022 Volume 75, Issue 1, Page(s) 130–136

Abstract: The alteration of pulmonary artery pressure is an important physiological indicator to reflect the organism's adaptation to acclimatization or the pathological injury in response to high-altitude hypoxic environment. The effects of hypoxic stress at ... ...

Abstract	The alteration of pulmonary artery pressure is an important physiological indicator to reflect the organism's adaptation to acclimatization or the pathological injury in response to high-altitude hypoxic environment. The effects of hypoxic stress at different altitudes for different time on pulmonary artery pressure are different. There are many factors involved in the changes of pulmonary artery pressure, such as the contraction of pulmonary arterial smooth muscle, hemodynamic changes, abnormal regulation of vascular activity and abnormal changes of cardiopulmonary function. Understanding of the regulatory factors of pulmonary artery pressure in hypoxic environment is crucial in clarifying the relevant mechanisms of hypoxic adaptation, acclimatization, prevention, diagnosis, treatment and prognosis of acute and chronic high-altitude diseases. In recent years, great progress has been made in the study regarding the factors affecting pulmonary artery pressure in response to high-altitude hypoxic stress. In this review, we discuss the regulatory factors and intervention measures of pulmonary arterial hypertension induced by hypoxia from the aspects of hemodynamics of circulatory system, vasoactive state and changes of cardiopulmonary function.
MeSH term(s)	Humans ; Altitude ; Arterial Pressure ; Acclimatization ; Hypoxia ; Muscle, Smooth
Language	Chinese
Publishing date	2022-11-03
Publishing country	China
Document type	Review ; English Abstract ; Journal Article
ZDB-ID	604308-2
ISSN	0371-0874
ISSN	0371-0874
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Zs.A 386: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (1.OG)
ab Jg. 2022: Lesesaal (EG)

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Article ; Online: Hypoxia-inducible factor-2 promotes liver fibrosis in non-alcoholic steatohepatitis liver disease via the NF-κB signalling pathway.

Cai, Hao / Bai, Zhenzhong / Ge, Ri-Li

Biochemical and biophysical research communications

2021 Volume 540, Page(s) 67–74

Abstract: Non-alcoholic steatohepatitis (NASH) is one of the most common chronic liver diseases. Chronic hypoxia is related to the pathogenesis of NASH. HIF-2α is the key gene for lipid metabolism, fibrosis, and inflammation in many cells. To identify the ... ...

Abstract	Non-alcoholic steatohepatitis (NASH) is one of the most common chronic liver diseases. Chronic hypoxia is related to the pathogenesis of NASH. HIF-2α is the key gene for lipid metabolism, fibrosis, and inflammation in many cells. To identify the molecular mechanism through which hypoxia exposure increases the morbidity of NASH, the expression level of HIF-2α was analysed and was found to be upregulated in human NASH liver. By constructing the NASH model of chronic hypoxia, the mice were housed at an altitude of 4300 m for 4 and 8 weeks, compared to the control groups that were housed at an altitude of 50 m. Histological studies showed that exposure to hypoxia promoted the activation of NF-κB by upregulating the expression of HIF-2α, as well as that of the genes related to inflammation and fibrosis, thereby promoting the development of NASH both in vivo and in vitro. In summary, hypoxia-exposure could upregulate HIF-2α to aggravate tissue fibrosis and inflammation by upregulating inflammation-related genes and fibrosis-related genes metabolites via the activated NF-κB pathway in NASH. Our results suggest that for NASH patients living at high altitudes, drug therapy could focus on treating tissue fibrosis and inflammation, and thus provides a new strategy for NASH treatment.
MeSH term(s)	Animals ; Basic Helix-Loop-Helix Transcription Factors/metabolism ; Disease Models, Animal ; Hep G2 Cells ; Humans ; Hypoxia/metabolism ; Inflammation/metabolism ; Liver/metabolism ; Liver/pathology ; Liver Cirrhosis/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; NF-kappa B/metabolism ; Non-alcoholic Fatty Liver Disease/metabolism ; Palmitates/pharmacology ; Signal Transduction ; Transcription Factor RelA/metabolism ; Up-Regulation
Chemical Substances	Basic Helix-Loop-Helix Transcription Factors ; NF-kappa B ; Palmitates ; Transcription Factor RelA ; endothelial PAS domain-containing protein 1 (1B37H0967P)
Language	English
Publishing date	2021-01-12
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	205723-2
ISSN	1090-2104 ; 0006-291X ; 0006-291X
ISSN (online)	1090-2104 ; 0006-291X
ISSN	0006-291X
DOI	10.1016/j.bbrc.2021.01.002
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Zs.A 116: Show issues

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Article ; Online: A Case of Human Hepatic Alveolar Echinococcosis Accompanied by Lung and Brain Metastases.

Liu, Chuanchuan / Fan, Haining / Ge, Ri-Li

The Korean journal of parasitology

2021 Volume 59, Issue 3, Page(s) 291–296

Abstract: Alveolar echinococcosis (AE) is considered as a fatal zoonosis caused by the larvae of Echinococcus multilocularis. The lungs and brain are the most common metastatic organs. We report a human case of hepatic alveolar echinococcosis accompanied by lung ... ...

Abstract	Alveolar echinococcosis (AE) is considered as a fatal zoonosis caused by the larvae of Echinococcus multilocularis. The lungs and brain are the most common metastatic organs. We report a human case of hepatic alveolar echinococcosis accompanied by lung and brain metastasis. In particular, the patient had a history of tuberculosis and the lung lesions were easily misdiagnosed as lung abscesses. The lesions of liver and lung underwent radical resection and confirmed as alveolar echinococcosis by pathological examination. The patient had no surgical complications after operation and was discharged after symptomatic treatment. Unfortunately, the patient later developed multiple intracerebral AE metastases. We required the patient to take albendazole orally for life and follow up.
MeSH term(s)	Animals ; Brain Neoplasms/diagnosis ; Echinococcosis ; Echinococcosis, Hepatic/diagnosis ; Echinococcosis, Hepatic/drug therapy ; Echinococcosis, Hepatic/surgery ; Echinococcus multilocularis ; Humans ; Lung/diagnostic imaging ; Lung/surgery ; Zoonoses
Language	English
Publishing date	2021-06-21
Publishing country	Korea (South)
Document type	Case Reports
ZDB-ID	286875-1
ISSN	1738-0006 ; 0023-4001
ISSN (online)	1738-0006
ISSN	0023-4001
DOI	10.3347/kjp.2021.59.3.291
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Zs.A 3476: Show issues

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ab Jg. 2022: Lesesaal (EG)

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Article: Brain-aging related protein expression and imaging characteristics of mice exposed to chronic hypoxia at high altitude.

Cao, Yaxin / Cao, Shundao / Ge, Ri-Li / Bao, Haihua / Mou, Yalin / Ji, Weizhong

Frontiers in aging neuroscience

2023 Volume 15, Page(s) 1268230

Abstract: Objective: To determine changes in protein expression related to brain aging and imaging features in mice after chronic hypoxia exposure at high altitude.: Method: A total of 24 healthy 4-week-old mice were randomly divided into high altitude hypoxia ...

Abstract	Objective: To determine changes in protein expression related to brain aging and imaging features in mice after chronic hypoxia exposure at high altitude. Method: A total of 24 healthy 4-week-old mice were randomly divided into high altitude hypoxia (HH) and plain control (PC) groups ( Results: The number of neuronal Nissl bodies in the hippocampus and frontal cortex was significantly decreased in the HH group compared to the PC group. Some hippocampal and frontal cortical neurons were apoptotic, the nuclei were wrinkled, chromatin was aggregated, and most mitochondria were mildly swollen (crista lysis, fracture). Compared with the PC group, the HH group showed elevated expression of caspase-3 mRNA, P16 mRNA, P21 mRNA, and P53 mRNA in the hippocampus and frontal cortex. Expression of Klotho mRNA in the frontal cortex was also significantly decreased. Western blot results showed that caspase-3 protein expression in the hippocampus and frontal cortex of the HH group was increased compared with the PC group. Moreover, there was decreased Klotho protein expression and significantly increased P-P53 protein expression. Compared with the PC group, expression of P16 protein in the frontal cortex of the HH group was increased and the gray matter (GM) volume in the left visceral area, left caudate nucleus, and left piriform cortex was decreased. Furthermore, the amplitude of low frequency fluctuation was decreased in the left posterior nongranular insular lobe, right small cell reticular nucleus, left flocculus, left accessory flocculus, and left primary auditory area, but increased in the GM layer of the left superior colliculus. Regional homogeneity was decreased in the left and right olfactory regions, but increased in the left bed nucleus. After exposure to high altitude, functional connectivity (FC) between the bilateral caudate nucleus and thalamus, corpus callosum, cingulate gyrus, anterior limbic cortex, globus pallidus, and hippocampus was weakened. FC between the right caudate nucleus and hypothalamus and entorhinal cortex was also weakened. The fractional anisotropy value of the left hippocampus was decreased in the HH group. Compared with the PC group, the HH group showed significantly increased inner diameters of the bilateral common carotid artery and left internal carotid artery. The cerebral blood flow values of the bilateral cortex and bilateral hippocampus in the HH group did not change significantly. Conclusion: Taken together, our findings show that chronic hypoxia exposure at high altitude may promote neuronal apoptosis and abnormal expression of related proteins, changing the structure and function of brain. These changes may contribute to brain aging.
Language	English
Publishing date	2023-10-02
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2558898-9
ISSN	1663-4365
ISSN	1663-4365
DOI	10.3389/fnagi.2023.1268230
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