Evidence map›Paper›PMID 36001204›Full record

ArticleMolecular and cellular biochemistry2023

Erythropoietin promotes energy metabolism to improve LPS-induced injury in HK-2 cells via SIRT1/PGC1-α pathway.

Kan Li, Li Gao, Sen Zhou, Yan-Rong Ma, Xiao Xiao, Qian Jiang, Zhi-Hong Kang, Ming-Long Liu, Tian-Xi Liu

Abstract read
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In one paragraph

Article in Molecular and cellular biochemistry, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
3.4field-weighted citation impact, top 6% 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

13 citing papers in PubMed, 22 citations in OpenAlex.

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  12. [Puerarin alleviates lipopolysaccharide-induced acute kidney injury in mice by modulating the SIRT1/NF-κB pathway].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2023
    Article
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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

9 authors at 2 institutions in 1 country.

Kan Li *Department of Nephrology, The First Hospital of Lanzhou University, No.1 Donggangxi Road, Chengguan District, Lanzhou, 730000, Gansu Province, China.
Li Gao *Department of Gynaecology, The First Hospital of Lanzhou University, Lanzhou, 730000, Gansu Province, China.
Sen Zhou *Department of Nephrology, The First Hospital of Lanzhou University, No.1 Donggangxi Road, Chengguan District, Lanzhou, 730000, Gansu Province, China.
Yan-Rong MaDepartment of Pharmacy, The First Hospital of Lanzhou University, Lanzhou, 730000, Gansu Province, China.
Xiao XiaoThe First Clinical Medical School of Lanzhou University, Lanzhou, 730000, Gansu Province, China.
Qian JiangThe First Clinical Medical School of Lanzhou University, Lanzhou, 730000, Gansu Province, China.
Zhi-Hong KangThe First Clinical Medical School of Lanzhou University, Lanzhou, 730000, Gansu Province, China.
Ming-Long LiuDepartment of Nephrology, The First Hospital of Lanzhou University, No.1 Donggangxi Road, Chengguan District, Lanzhou, 730000, Gansu Province, China.
Tian-Xi LiuDepartment of Nephrology, The First Hospital of Lanzhou University, No.1 Donggangxi Road, Chengguan District, Lanzhou, 730000, Gansu Province, China. liutianxildyy@163.com.ORCID http://orcid.org/0000-0002-3279-8876
First Hospital of Lanzhou University · CNLanzhou University · CN

Funding

National Natural Science Foundation of Gansu Province Grant No. 20JR5RA350
6 · The paper itself

Abstract

Acute kidney injury (AKI) is one of frequent complications of sepsis with high mortality. Mitochondria is the center of energy metabolism participating in the pathogenesis of sepsis-associated AKI, and SIRT1/PGC1-α signaling pathway plays a crucial role in the modulation of energy metabolism. Erythropoietin (EPO) exerts protective functions on chronic kidney disease. We aimed to assess the effects of EPO on cell damage and energy metabolism in a cell model of septic AKI. Renal tubular epithelial cells HK-2 were treated with LPS and human recombinant erythropoietin (rhEPO). Cell viability was detected by CCK-8 and mitochondrial membrane potential was determined using JC-1 fluorescent probe. Then the content of ATP, ADP and NADPH, as well as lactic acid, were measured for the assessment of energy metabolism. Oxidative stress was evaluated by detecting the levels of ROS, MDA, SOD and GSH. Pro-inflammatory cytokines, including TNF-α, IL-6, and IL-1β, were measured with ELISA. Moreover, qRT-PCR and western blot were performed to detect mRNA and protein expressions. shSIRT1 was used to knockdown SIRT1, while EX527 and SR-18292 were applied to inhibit SIRT1 and PGC1-α, respectively, to investigate the regulatory mechanism of rhEPO on inflammatory injury and energy metabolism. In LPS-exposed HK-2 cells, rhEPO attenuated cell damage, inflammation and abnormal energy metabolism, as indicated by the elevated cell viability, the inhibited oxidative stress, cell apoptosis and inflammation, as well as the increased mitochondrial membrane potential and energy metabolism. However, these protective effects induced by rhEPO were reversed after SIRT1 or PGC1-α inhibition. EPO activated SIRT1/PGC1-α pathway to alleviate LPS-induced abnormal energy metabolism and cell damage in HK-2 cells. Our study suggested that rhEPO played a renoprotective role through SIRT1/PGC1-α pathway, which supported its therapeutic potential in septic AKI.

Indexed as

Acute Kidney InjuryErythropoietinSepsisApoptosisEnergy MetabolismHumansInflammationKidneyLipopolysaccharidesSirtuin 1ErythropoietinLipopolysaccharidesSIRT1 protein, humanSirtuin 1Energy metabolismErythropoietinHK-2 cellsLPSPGC1-αRenoprotectionSIRT1

Identifiers

PMID36001204
OpenAlexW4293169229

What OpenQuestion holds

Textmetadata
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.