Evidence map›Paper›PMID 34956478›Full record

ArticleAmerican journal of translational research2021

The roles of AMPK-mediated autophagy and mitochondrial autophagy in a mouse model of imiquimod-induced psoriasis.

Hui Shen, Yan Sha, Jun Huang, An-Qi Mao, Tao Zhang, Mu-Yao Wu, Fang Sun, Ying-Yuan Yu, Zhong-Qin Cheng, Ya-Ting Gong

Open access · greenAbstract read
In one paragraph

Article in American journal of translational research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.0field-weighted citation impact, top 13% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

17 citing papers in PubMed, 16 citations in OpenAlex.

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  15. The Role of Adipokines in the Pathogenesis of Psoriasis.International journal of molecular sciences · 2023
    Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors at 3 institutions in 1 country.

Hui ShenDepartment of Dermatology, Zhangjiagang TCM Hospital Affiliated to Nanjing University of Chinese Medicine Zhangjiagang 215600, Jiangsu, China.
Yan ShaDepartment of Dermatology, Zhangjiagang TCM Hospital Affiliated to Nanjing University of Chinese Medicine Zhangjiagang 215600, Jiangsu, China.
Jun HuangDepartment of Dermatology, Zhangjiagang TCM Hospital Affiliated to Nanjing University of Chinese Medicine Zhangjiagang 215600, Jiangsu, China.
An-Qi MaoDepartment of Dermatology, Zhangjiagang TCM Hospital Affiliated to Nanjing University of Chinese Medicine Zhangjiagang 215600, Jiangsu, China.
Tao ZhangDepartment of Acupuncture, Zhangjiagang TCM Hospital Affiliated to Nanjing University of Chinese Medicine Zhangjiagang 215600, Jiangsu, China.
Mu-Yao WuDepartment of Rehabilitation, Zhangjiagang TCM Hospital Affiliated to Nanjing University of Chinese Medicine Zhangjiagang 215600, Jiangsu, China.
Fang SunDepartment of Dermatology, Aoyang Hospital Affiliated to Jiangsu University Zhangjiagang 215600, Jiangsu, China.
Ying-Yuan YuDepartment of Dermatology, Nanjing Medical University Nanjing 210029, Jiangsu, China.
Zhong-Qin ChengDepartment of Dermatology, Zhangjiagang TCM Hospital Affiliated to Nanjing University of Chinese Medicine Zhangjiagang 215600, Jiangsu, China.
Ya-Ting GongDepartment of Rehabilitation, Zhangjiagang TCM Hospital Affiliated to Nanjing University of Chinese Medicine Zhangjiagang 215600, Jiangsu, China.
Nanjing University of Chinese Medicine · CNNanjing Medical University · CNSoochow University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundPsoriasis is a systemic inflammatory disease characterized by epidermal hyperplasia and skin inflammatory infiltrates. Inactivation of AMPK has been shown to decrease autophagy, thereby inhibiting elimination of inflammatory factors and harmful substances, and aggravating psoriasis. However, the molecular mechanism through which AMPK affects psoriasis remains to be further explored. In this study, we investigated whether AMPK regulates autophagy through the ULK1/Atg7 signaling pathway and regulates mitochondrial autophagy through the PINK1/Parkin signaling pathway, thereby affecting a mouse model of psoriasis.

methodsImiquimod was used to induce psoriasis-like lesions on the backs of mice. The severity of skin lesions in psoriatic mice was evaluated with the skin inflammation severity score, and epidermal thickness was measured on the basis of H&E staining. RT-PCR, western blotting and immunofluorescence staining were used to detect indicators of autophagy and mitochondrial autophagy.

resultsAMPK activity was inhibited in the psoriasis mouse model, the autophagy-associated proteins ULK1/Atg7 were inhibited, and the mitochondrial autophagy proteins PINK1/Parkin were also decreased. Results indicated that autophagy and mitochondrial autophagy were inhibited in the mouse model. When AMPK signaling was upregulated, ULK1/Atg7 and PINK1/Parkin were upregulated, autophagy and mitochondrial autophagy increased, and skin lesions in the mouse model were alleviated. ULK1/Atg7 and PINK1/Parkin were down-regulated when AMPK signaling was downregulated, and psoriasis-like skin lesions were aggravated in mice. These results indicated that AMPK regulates autophagy through the ULK1/Atg7 signaling pathway and regulates mitochondrial autophagy through the PINK1/Parkin signaling pathway, thus affecting the prognosis of psoriasis in the mouse model.

conclusionAMPK affects the prognosis of psoriasis in a mouse model by regulating autophagy and mitochondrial autophagy.

Indexed as

AMPKautophagymitochondrial autophagyPINK1psoriasisULK1

Identifiers

PMID34956478
PMCPMC8661142
OpenAlexW4206851314

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.