miR-34a promotes liver fibrosis in patients with chronic hepatitis via mediating Sirt1/p53 signaling pathway

Li, Xiaojie; Zhang, Weiying; Xu, Kun; Lu, Jing

doi:10.1016/j.prp.2020.152876

Cited by 20 publications

(36 citation statements)

References 25 publications

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“…MiRNA‐34a (miRNA‐34a) is a well‐known miRNA regulated by p53. Similar to p53, miRNA‐34a promotes lung 15 and liver 16 fibrosis. An Italian group determines that many miRNAs, including miRNA‐34a, are up‐regulated in the serum of neovascular AMD patients 17 .…”

Section: Introductionmentioning

confidence: 98%

The HIF‐1α/p53/miRNA‐34a/Klotho axis in retinal pigment epithelial cells promotes subretinal fibrosis and exacerbates choroidal neovascularization

Xie

Wáng

et al. 2021

J Cellular Molecular Medi

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Wet age‐related macular degeneration (wAMD), characterized by choroidal neovascularization (CNV), is a leading cause of irreversible vision loss among elderly people in developed nations. Subretinal fibrosis, mediated by epithelial‐mesenchymal transition (EMT) of retinal pigment epithelium (RPE) cells, leads to unsuccessful anti‐vascular endothelial growth factor (VEGF) agent treatments in CNV patients. Under hypoxic conditions, hypoxia‐inducible factor‐1α (HIF‐1α) increases the stability and activation of p53, which activates microRNA‐34a (miRNA‐34a) transcription to promote fibrosis. Additionally, Klotho is a target gene of miRNA‐34a that inhibits fibrosis. This study aimed to explore the role of the HIF‐1α/p53/miRNA‐34a/Klotho axis in subretinal fibrosis and CNV. Hypoxia‐induced HIF‐1α promoted p53 stability, phosphorylation and nuclear translocation in ARPE‐19 cells (a human RPE cell line). HIF‐1α‐dependent p53 activation up‐regulated miRNA‐34a expression in ARPE‐19 cells following hypoxia. Moreover, hypoxia‐induced p53‐dependent miRNA‐34a inhibited the expression of Klotho in ARPE‐19 cells. Additionally, the HIF‐1α/p53/miRNA‐34a/Klotho axis facilitated hypoxia‐induced EMT in ARPE‐19 cells. In vivo, blockade of the HIF‐1α/p53/miRNA‐34a/Klotho axis alleviated the formation of mouse laser‐induced CNV and subretinal fibrosis. In short, the HIF‐1α/p53/miRNA‐34a/Klotho axis in RPE cells promoted subretinal fibrosis, thus aggravating the formation of CNV.

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Section: Introductionmentioning

confidence: 98%

The HIF‐1α/p53/miRNA‐34a/Klotho axis in retinal pigment epithelial cells promotes subretinal fibrosis and exacerbates choroidal neovascularization

Xie

Wáng

et al. 2021

J Cellular Molecular Medi

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“…The influence of SIRT1 action in the development of CHC has been demonstrated. Li et al [25] showed a significantly lower SIRT1 expression and increased levels of acetylated p53 in the liver tissues of CHC patients compared to the healthy controls. The decrease in SIRT1 expression was correlated with increased serum levels miR-34a and ac-p53, which suggests that SIRT1 may be inhibited by miR-34a, promoting apoptotic processes in hepatocytes [25].…”

Section: Liver Disturbances In Hiv and Sirtuin's Rolementioning

confidence: 99%

“…Among HIV-positive patients, hepatitis B virus (HBV) and hepatitis C virus (HCV) co-infection are common, which significantly increases the risk of liver cirrhosis and fibrosis. It is estimated that HCV co-infection occurs in approximately 5.8% of HIV-infected people [25]. Liver fibrosis is a reversible condition, caused by the activation of HSCs by platelet-derived growth factor (PDGF) or transforming growth factor β (TGF-β).…”

Section: Liver Disturbances In Hiv and Sirtuin's Rolementioning

confidence: 99%

Sirtuins as Interesting Players in the Course of HIV Infection and Comorbidities

Jurkowska

Szymańska

Knysz

et al. 2021

Cells

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The sirtuins (SIRTs) are a family of enzymes from the group of NAD+-dependent deacetylases. Through the reaction of splitting the acetyl group of various transcription factors and histones they regulate many processes in the organism. The activity of sirtuins is linked to metabolic control, oxidative stress, inflammation and apoptosis, and they also affect the course of viral infections. For this reason, they may participate in the pathogenesis and development of many diseases, but little is known about their role in the course of human immunodeficiency virus (HIV) infection, which is the subject of this review. In the course of HIV infection, comorbidities such as: neurodegenerative disorders, obesity, insulin resistance and diabetes, lipid disorders and cardiovascular diseases, renal and bone diseases developed more frequently and faster compared to the general population. The role of sirtuins in the development of accompanying diseases in the course of HIV infection may also be interesting. There is still a lack of detailed information on this subject. The role of sirtuins, especially SIRT1, SIRT3, SIRT6, are indicated to be of great importance in the course of HIV infection and the development of the abovementioned comorbidities.

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“…Specific blocking of Smad3 protein expression may inhibit liver fibrosis (13). MicroRNA consists of 21-25 nucleotides (14), and is involved in the shearing of message RNA (mRNA), inhibiting or enhancing the expression of its regulatory genes in the translation process, so as to participate in the processes of ontogeny, body metabolism, as well as the occurrence and development of diseases (15)(16)(17).…”

Section: Original Articlementioning

confidence: 99%

MiR-34a promotes fibrosis of hepatic stellate cells via the TGF-β pathway

Zhang¹,

Wang²,

Yao³

et al. 2021

Ann Transl Med

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miR-34a promotes liver fibrosis in patients with chronic hepatitis via mediating Sirt1/p53 signaling pathway

Cited by 20 publications

References 25 publications

The HIF‐1α/p53/miRNA‐34a/Klotho axis in retinal pigment epithelial cells promotes subretinal fibrosis and exacerbates choroidal neovascularization

The HIF‐1α/p53/miRNA‐34a/Klotho axis in retinal pigment epithelial cells promotes subretinal fibrosis and exacerbates choroidal neovascularization

Sirtuins as Interesting Players in the Course of HIV Infection and Comorbidities

MiR-34a promotes fibrosis of hepatic stellate cells via the TGF-β pathway

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