Tubular epithelial cell-derived extracellular vesicles induce macrophage glycolysis by stabilizing HIF-1α in diabetic kidney disease

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Location: Deutsche Nationalbibliothek Frankfurt am Main

ISSN: 1528-3658

Extent: Online-Ressource

Language: Englisch

Notes: online resource.

Bibliographic citation: Tubular epithelial cell-derived extracellular vesicles induce macrophage glycolysis by stabilizing HIF-1α in diabetic kidney disease ; volume:28 ; number:1 ; day:12 ; month:8 ; year:2022 ; pages:1-11 ; date:12.2022
Molecular medicine ; 28, Heft 1 (12.8.2022), 1-11, 12.2022

Creator: Jia, Yijie
Chen, Jiaqi
Zheng, Zhikang
Tao, Yuan
Zhang, Shuting
Zou, Meina
Yang, Yanlin
Xue, Meng
Hu, Fang
Li, Yang
Zhang, Qian
Xue, Yaoming
Zheng, Zongji

Contributor: SpringerLink (Online service)

DOI: 10.1186/s10020-022-00525-1

URN: urn:nbn:de:101:1-2022112709510466816574

Rights: Open Access; Der Zugriff auf das Objekt ist unbeschränkt möglich.

Last update: 15.08.2025, 7:27 AM CEST

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Associated

Jia, Yijie
Chen, Jiaqi
Zheng, Zhikang
Tao, Yuan
Zhang, Shuting
Zou, Meina
Yang, Yanlin
Xue, Meng
Hu, Fang
Li, Yang
Zhang, Qian
Xue, Yaoming
Zheng, Zongji
SpringerLink (Online service)

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Hochschulschrift

Small molecules stabilizing HIF-α [HIF-alpha] by PHD inhibition

MAT1A activation of glycolysis to promote NSCLC progression depends on stabilizing CCND1

ALKBH1 promotes HIF-1α-mediated glycolysis by inhibiting N-glycosylation of LAMP2A

SOD3 improves the tumor response to chemotherapy by stabilizing endothelial HIF-2α

Differentiated kidney tubular cell-derived extracellular vesicles enhance maturation of tubuloids

Ulinastatin attenuates renal fibrosis by regulating AMPK/HIF-1α signaling pathway-mediated glycolysis

Exogenous acetate attenuates inflammatory responses through HIF-1α-dependent glycolysis regulation in macrophage

LncRNA SNHG11 facilitates tumor metastasis by interacting with and stabilizing HIF-1α

Testosterone induces renal tubular epithelial cell death through the HIF-1α/BNIP3 pathway

Renal Tubular HIF-2α Expression Requires VHL Inactivation and Causes Fibrosis and Cysts

NPAS2 promotes aerobic glycolysis and tumor growth in prostate cancer through HIF-1A signaling

Docetaxel suppressed cell proliferation through Smad3/HIF-1α-mediated glycolysis in prostate cancer cells

Hochschulschrift

Small molecules stabilizing HIF-α [HIF-alpha] by PHD inhibition

MAT1A activation of glycolysis to promote NSCLC progression depends on stabilizing CCND1

ALKBH1 promotes HIF-1α-mediated glycolysis by inhibiting N-glycosylation of LAMP2A

SOD3 improves the tumor response to chemotherapy by stabilizing endothelial HIF-2α

Differentiated kidney tubular cell-derived extracellular vesicles enhance maturation of tubuloids

Ulinastatin attenuates renal fibrosis by regulating AMPK/HIF-1α signaling pathway-mediated glycolysis

Exogenous acetate attenuates inflammatory responses through HIF-1α-dependent glycolysis regulation in macrophage

LncRNA SNHG11 facilitates tumor metastasis by interacting with and stabilizing HIF-1α

Testosterone induces renal tubular epithelial cell death through the HIF-1α/BNIP3 pathway

Renal Tubular HIF-2α Expression Requires VHL Inactivation and Causes Fibrosis and Cysts

NPAS2 promotes aerobic glycolysis and tumor growth in prostate cancer through HIF-1A signaling

Docetaxel suppressed cell proliferation through Smad3/HIF-1α-mediated glycolysis in prostate cancer cells

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Tubular epithelial cell-derived extracellular vesicles induce macrophage glycolysis by stabilizing HIF-1α in diabetic kidney disease

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Other Objects (12)

Small molecules stabilizing HIF-α [HIF-alpha] by PHD inhibition

MAT1A activation of glycolysis to promote NSCLC progression depends on stabilizing CCND1

ALKBH1 promotes HIF-1α-mediated glycolysis by inhibiting N-glycosylation of LAMP2A

SOD3 improves the tumor response to chemotherapy by stabilizing endothelial HIF-2α

Differentiated kidney tubular cell-derived extracellular vesicles enhance maturation of tubuloids

Ulinastatin attenuates renal fibrosis by regulating AMPK/HIF-1α signaling pathway-mediated glycolysis

Exogenous acetate attenuates inflammatory responses through HIF-1α-dependent glycolysis regulation in macrophage

LncRNA SNHG11 facilitates tumor metastasis by interacting with and stabilizing HIF-1α

Testosterone induces renal tubular epithelial cell death through the HIF-1α/BNIP3 pathway

Renal Tubular HIF-2α Expression Requires VHL Inactivation and Causes Fibrosis and Cysts

NPAS2 promotes aerobic glycolysis and tumor growth in prostate cancer through HIF-1A signaling

Docetaxel suppressed cell proliferation through Smad3/HIF-1α-mediated glycolysis in prostate cancer cells

Small molecules stabilizing HIF-α [HIF-alpha] by PHD inhibition

MAT1A activation of glycolysis to promote NSCLC progression depends on stabilizing CCND1

ALKBH1 promotes HIF-1α-mediated glycolysis by inhibiting N-glycosylation of LAMP2A

SOD3 improves the tumor response to chemotherapy by stabilizing endothelial HIF-2α

Differentiated kidney tubular cell-derived extracellular vesicles enhance maturation of tubuloids

Ulinastatin attenuates renal fibrosis by regulating AMPK/HIF-1α signaling pathway-mediated glycolysis

Exogenous acetate attenuates inflammatory responses through HIF-1α-dependent glycolysis regulation in macrophage

LncRNA SNHG11 facilitates tumor metastasis by interacting with and stabilizing HIF-1α

Testosterone induces renal tubular epithelial cell death through the HIF-1α/BNIP3 pathway

Renal Tubular HIF-2α Expression Requires VHL Inactivation and Causes Fibrosis and Cysts

NPAS2 promotes aerobic glycolysis and tumor growth in prostate cancer through HIF-1A signaling

Docetaxel suppressed cell proliferation through Smad3/HIF-1α-mediated glycolysis in prostate cancer cells

Small molecules stabilizing HIF-α [HIF-alpha] by PHD inhibition

MAT1A activation of glycolysis to promote NSCLC progression depends on stabilizing CCND1

ALKBH1 promotes HIF-1α-mediated glycolysis by inhibiting N-glycosylation of LAMP2A

SOD3 improves the tumor response to chemotherapy by stabilizing endothelial HIF-2α

Differentiated kidney tubular cell-derived extracellular vesicles enhance maturation of tubuloids

Ulinastatin attenuates renal fibrosis by regulating AMPK/HIF-1α signaling pathway-mediated glycolysis

Exogenous acetate attenuates inflammatory responses through HIF-1α-dependent glycolysis regulation in macrophage

LncRNA SNHG11 facilitates tumor metastasis by interacting with and stabilizing HIF-1α

Testosterone induces renal tubular epithelial cell death through the HIF-1α/BNIP3 pathway

Renal Tubular HIF-2α Expression Requires VHL Inactivation and Causes Fibrosis and Cysts

NPAS2 promotes aerobic glycolysis and tumor growth in prostate cancer through HIF-1A signaling

Docetaxel suppressed cell proliferation through Smad3/HIF-1α-mediated glycolysis in prostate cancer cells

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