Mitochondria-targeted reactive oxygen species blockor SS-31 blocks hepatic
stellate cell activation and alleviates hepatic fibrosis by regulating NLRP3
inflammasomes

Li  Liu,; YingFeng  Wei,; NingSheng  Xie,; Hong  Cai,; Ye Lin,

doi:10.14715/cmb/2024.70.2.25

Cell Mol Biol (Noisy-le-grand)

2024

DOI: 10.14715/cmb/2024.70.2.25

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Mitochondria-targeted reactive oxygen species blockor SS-31 blocks hepatic stellate cell activation and alleviates hepatic fibrosis by regulating NLRP3 inflammasomes

Li Liu,

YingFeng Wei,

NingSheng Xie

et al.

Abstract: , and intracellular ROS can cause NLRP3 inflammasome activation [18][19][20].An aromatic cationic peptide, Szeto-Schiller (SS)-31 peptide, scavenges hydrogen peroxide, superoxide,

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Cited by 3 publications

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Modulation of Redox Metabolism, CD147, and CD47 Expression with the Maturation of Hematopoietic Stem Cells in Bone Marrow

Bhardwaj,

Singh,

Babu

et al. 2024

Indian J Hematol Blood Transfus

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Modulation of Redox Metabolism, CD147, and CD47 Expression with the Maturation of Hematopoietic Stem Cells in Bone Marrow

Bhardwaj,

Singh,

Babu

et al. 2024

Indian J Hematol Blood Transfus

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CCL4/CCR5 regulates chondrocyte biology and OA progression

Deng,

Xue,

Zhou

et al. 2024

Cytokine

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The effects of TGF-β-induced activation and starvation of vitamin A and palmitic acid on human stem cell-derived hepatic stellate cells

Wilhelmsen,

Combriat,

Dalmao-Fernandez

et al. 2024

Stem Cell Res Ther

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Background Hepatic stellate cells (HSC) have numerous critical roles in liver function and homeostasis, while they are also known for their importance during liver injury and fibrosis. There is therefore a need for relevant in vitro human HSC models to fill current knowledge gaps. In particular, the roles of vitamin A (VA), lipid droplets (LDs), and energy metabolism in human HSC activation are poorly understood. Methods In this study, human pluripotent stem cell-derived HSCs (scHSCs), benchmarked to human primary HSC, were exposed to 48-hour starvation of retinol (ROL) and palmitic acid (PA) in the presence or absence of the potent HSC activator TGF-β. The interventions were studied by an extensive set of phenotypic and functional analyses, including transcriptomic analysis, measurement of activation-related proteins and cytokines, VA- and LD storage, and cell energy metabolism. Results The results show that though the starvation of ROL and PA alone did not induce scHSC activation, the starvation amplified the TGF-β-induced activation-related transcriptome. However, TGF-β-induced activation alone did not lead to a reduction in VA or LD stores. Additionally, reduced glycolysis and increased mitochondrial fission were observed in response to TGF-β. Conclusions scHSCs are robust models for activation studies. The loss of VA and LDs is not sufficient for scHSC activation in vitro, but may amplify the TGF-β-induced activation response. Collectively, our work provides an extensive framework for studying human HSCs in healthy and diseased conditions.

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Mitochondria-targeted reactive oxygen species blockor SS-31 blocks hepatic stellate cell activation and alleviates hepatic fibrosis by regulating NLRP3 inflammasomes

Abstract: , and intracellular ROS can cause NLRP3 inflammasome activation [18][19][20].An aromatic cationic peptide, Szeto-Schiller (SS)-31 peptide, scavenges hydrogen peroxide, superoxide,

Cited by 3 publications

References 36 publications

Modulation of Redox Metabolism, CD147, and CD47 Expression with the Maturation of Hematopoietic Stem Cells in Bone Marrow

Modulation of Redox Metabolism, CD147, and CD47 Expression with the Maturation of Hematopoietic Stem Cells in Bone Marrow

CCL4/CCR5 regulates chondrocyte biology and OA progression

The effects of TGF-β-induced activation and starvation of vitamin A and palmitic acid on human stem cell-derived hepatic stellate cells

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