Evidence map›Paper›PMID 36882837›Full record

ArticleLipids in health and disease2023

Exercise activates Sirt1-mediated Drp1 acetylation and inhibits hepatocyte apoptosis to improve nonalcoholic fatty liver disease.

Zongqiang Hu, Hongyu Zhang, Yiting Wang, Boyi Li, Kaiyu Liu, Jianghua Ran, Li Li

Open access · goldAbstract read
In one paragraph

Article in Lipids in health and disease, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
5.1field-weighted citation impact, top 4% 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

23 citing papers in PubMed, 24 citations in OpenAlex.

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  17. Nrf2 mediated signaling axis in sepsis-induced cardiomyopathy: potential Pharmacological receptor.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025
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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

7 authors at 3 institutions in 1 country.

Zongqiang HuFirst People's Hospital of Kunming City, The Calmette Affiliated Hospital of Kunming Medical University, Kunming, Yunnan, China.
Hongyu ZhangFirst People's Hospital of Kunming City, The Calmette Affiliated Hospital of Kunming Medical University, Kunming, Yunnan, China.
Yiting WangFirst People's Hospital of Kunming City, The Calmette Affiliated Hospital of Kunming Medical University, Kunming, Yunnan, China.
Boyi LiFirst People's Hospital of Kunming City, The Calmette Affiliated Hospital of Kunming Medical University, Kunming, Yunnan, China.
Kaiyu LiuFirst People's Hospital of Kunming City, The Calmette Affiliated Hospital of Kunming Medical University, Kunming, Yunnan, China.
Jianghua RanFirst People's Hospital of Kunming City, The Calmette Affiliated Hospital of Kunming Medical University, Kunming, Yunnan, China. ranjianghua@kmmu.edu.cn.
Li LiFirst People's Hospital of Kunming City, The Calmette Affiliated Hospital of Kunming Medical University, Kunming, Yunnan, China. lili6@kmmu.edu.cn.
Kunming Medical University · CNThe First Hospital of Kunming · CNFirst Affiliated Hospital of Kunming Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeAerobic exercise has shown beneficial effects in the prevention and treatment of non-alcoholic fatty liver disease (NAFLD). Nevertheless, the regulatory mechanism is not turely clear. Therefore, we aim to clarify the possible mechanism by investigating the effects of aerobic exercise on NAFLD and its mitochondrial dysfunction.

methodsNAFLD rat model was established by feeding high fat diet. and used oleic acid (OA) to treat HepG2 cells. Changes in histopathology, lipid accumulation, apoptosis, body weight, and biochemical parameters were assessed. In addition, antioxidants, mitochondrial biogenesis and mitochondrial fusion and division were assessed.

resultsThe obtained in vivo results showed that aerobic exercise significantly improved lipid accumulation and mitochondrial dysfunction induced by HFD, activated the level of Sirtuins1 (Srit1), and weakened the acetylation and activity of dynamic-related protein 1 (Drp1). In vitro results showed that activation of Srit1 inhibited OA-induced apoptosis in HepG2 cells and alleviated OA-induced mitochondrial dysfunction by inhibiting Drp1 acetylation and reducing Drp1 expression.

conclusionAerobic exercise alleviates NAFLD and its mitochondrial dysfunction by activating Srit1 to regulate Drp1 acetylation. Our study clarifies the mechanism of aerobic exercise in alleviating NAFLD and its mitochondrial dysfunction and provides a new method for adjuvant treatment of NAFLD.

Indexed as

DynaminsNon-alcoholic Fatty Liver DiseaseSirtuin 1AcetylationAnimalsApoptosisHepatocytesHep G2 CellsHumansOleic AcidPhysical Conditioning, AnimalRatsDNM1L protein, humanDnm1l protein, ratDynaminsOleic AcidSIRT1 protein, humanSirt1 protein, ratSirtuin 1Aerobic exerciseDrp1 acetylationMitochondrial dysfunctionNAFLDSrit1

Identifiers

PMID36882837
PMCPMC9990292
OpenAlexW4323362319

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.