Evidence map›Paper›PMID 31524263›Full record

ArticleMolecular medicine reports2019

Alleviation of sepsis‑induced cardiac dysfunction by overexpression of Sestrin2 is associated with inhibition of p‑S6K and activation of the p‑AMPK pathway.

Ziwen Wang, Lin Bu, Peng Yang, Shoujie Feng, Feng Xu

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Molecular medicine reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.1field-weighted citation impact, top 12% 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

20 citing papers in PubMed, 37 citations in OpenAlex.

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  18. Sestrins in Physiological Stress Responses.Annual review of physiology · 2021
    Review
  19. Exploring the beneficial role of telmisartan in sepsis-induced myocardial injury through inhibition of high-mobility group box 1 and glycogen synthase kinase-3β/nuclear factor-κB pathway.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2020
    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

5 authors at 3 institutions in 1 country.

Ziwen WangDepartment of Emergency Surgery, The First Affiliated Hospital of Soochow University, Suzhou, Jiangsu 215006, P.R. China.
Lin BuIntensive Care Unit, The Affiliated Hospital of Xuzhou Medical University, Xuzhou, Jiangsu 221000, P.R. China.
Peng YangDepartment of Emergency Surgery, The First Affiliated Hospital of Soochow University, Suzhou, Jiangsu 215006, P.R. China.
Shoujie FengDepartment of Thoracic Surgery, The Affiliated Hospital of Xuzhou Medical University, Xuzhou, Jiangsu 221000, P.R. China.
Feng XuDepartment of Emergency Surgery, The First Affiliated Hospital of Soochow University, Suzhou, Jiangsu 215006, P.R. China.
Soochow University · CNXuzhou Medical College · CNFirst Affiliated Hospital of Soochow University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Sepsis‑induced myocardial injury is one of the manifestations of multiple organ dysfunction in sepsis. The aim of the present study was to determine the mechanism of alleviation of lipopolysaccharide (LPS)‑induced injury on cardiomyocytes by Sestrin2. A sepsis model using LPS injection was constructed in Sprague‑Dawley (SD) rats, and after 6, 12 and 24 h, rat blood was collected and cardiac troponin T (CTnT) levels were determined using ELISA. Heart specimens were excised, tumor necrosis factor‑α (TNF‑α) and interleukin 6 (IL‑6) levels were detected by ELISA, malondialdehyde (MDA) levels were estimated using colorimetric analysis, and phosphorylated (p)‑S6K and p‑AMP‑activated protein kinase (AMPK) levels were determined by western blot analysis. In the septic rats, phenomenon of myocardial fiber rupture, interstitial edema and inflammatory cell infiltration were observed under light microscope. Following LPS injection, CTnT in serum and MDA in myocardial homogenate were increased time‑dependently. TNF‑α and IL‑6 levels were significantly increased, with a peak at 6 h. p‑S6K levels were adaptively downregulated, and levels of p‑AMPK and Sestrin2 were adaptively upregulated by LPS. In LPS‑injured H9c2 cells, Sestrin2 overexpression attenuated the LPS‑mediated inhibitory effects on cell viability, suppressed LPS‑mediated increase in CTnT, TNF‑α, IL‑6 and MDA levels, as well as attenuated p‑S6K levels and elevated p‑AMPK and Sestrin2 levels. Sestrin2 interference showed the opposite effect. Sestrin2 promoted cell viability and inhibited the inflammatory responses of LPS‑injured myocardial cells. The phenomena may be associated with inhibition of p‑S6K and activation of the p‑AMPK pathway.

Indexed as

AMP-Activated Protein KinasesAnimalsCell SurvivalFemaleGene ExpressionHeart DiseasesLipopolysaccharidesMyocardiumMyocytes, CardiacNuclear ProteinsRatsRibosomal Protein S6 Kinases, 70-kDaSepsisSestrinsSignal TransductionAMP-Activated Protein KinasesLipopolysaccharidesNuclear ProteinsRibosomal Protein S6 Kinases, 70-kDaSesn2 protein, ratSestrins

Identifiers

PMID31524263
PMCPMC6691248
OpenAlexW2963087554

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.