Evidence map›Paper›PMID 36259464›Full record

ArticleRenal failure2022

Regulation of the autophagy plays an important role in acute kidney injury induced acute lung injury.

Ruolin Wang, Siheng Shen, Luyong Jian, Shuhua Liu, Qi Yuan, Huahui Guo, Jiasheng Huang, Penghui Chen, Renfa Huang

Open access · goldAbstract read
In one paragraph

Article in Renal failure, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
0.1field-weighted citation impact, top 50% 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

0 citing papers in PubMed, 1 citations in OpenAlex.

No citing paper in PubMed yet.

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 1 institution in 1 country.

Ruolin WangNephropathy Department, Shenzhen Hospital (Futian) of Guangzhou University of Chinese Medicine, Shenzhen, China.ORCID 0000-0002-0348-5256
Siheng ShenNephropathy Department, Shenzhen Hospital (Futian) of Guangzhou University of Chinese Medicine, Shenzhen, China.ORCID 0000-0002-3505-6683
Luyong JianNephropathy Department, Shenzhen Hospital (Futian) of Guangzhou University of Chinese Medicine, Shenzhen, China.ORCID 0000-0001-9233-4961
Shuhua LiuThe Third Clinical Medical School, Guangzhou University of Chinese Medicine, Guangzhou, China.ORCID 0000-0002-8633-5826
Qi YuanNephropathy Department, Shenzhen Hospital (Futian) of Guangzhou University of Chinese Medicine, Shenzhen, China.ORCID 0000-0002-7040-4612
Huahui GuoNephropathy Department, Shenzhen Hospital (Futian) of Guangzhou University of Chinese Medicine, Shenzhen, China.ORCID 0000-0003-1106-5312
Jiasheng HuangNephropathy Department, Shenzhen Hospital (Futian) of Guangzhou University of Chinese Medicine, Shenzhen, China.
Penghui ChenNephropathy Department, Shenzhen Hospital (Futian) of Guangzhou University of Chinese Medicine, Shenzhen, China.ORCID 0000-0001-8252-936X
Renfa HuangNephropathy Department, Shenzhen Hospital (Futian) of Guangzhou University of Chinese Medicine, Shenzhen, China.ORCID 0000-0003-3096-4129
Guangzhou University of Chinese Medicine · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimThis study aimed to investigate the regulatory role of autophagy in acute kidney injury (AKI) induced acute lung injury (ALI).

methodsThe male Sprague-Dawley rats were divided into four groups: normal saline-treated sham rats (sham group), normal saline-treated ischemia-reperfusion injury rats (IRI group), 3-methyladenine-treated IRI rats (3-MA group), and rapamycin-treated IRI rats (RA group). The rats in the IRI rat model received the nephrectomy of the right kidney and was subjected to 60 mins of left renal pedicle occlusion, followed by 12, 24, 48, and 72 h of reperfusion. The levels of Scr, BUN, wet-to-dry ratio of lung, inflammatory cytokines, and oxidative stress were determined. The damage to tissues was detected by histological examinations. The western blot and immunohistochemistry methods were conducted to determine the expression of indicated proteins.

resultsRenal IRI could induce the pulmonary injury after AKI, which caused significant increases in the function index of pulmonary and renal, the levels of inflammatory cytokines, and biomarkers of oxidative stress. In comparison to the IRI group, the RA group showed significantly decreased P62 and Caspase-3 expression and increased LC-II/LC3-I, Beclin-1, Bcl-2, and unc-51-like autophagy activating kinase 1 expression. Meanwhile, by suppressing the inflammation and oxidative stress, as well as inhibiting the pathological lesions in kidney and lung tissues, the autophagy could effectively ameliorate IRI-induced AKI and ALI.

conclusionsAutophagy plays an important role in AKI-induced ALI, which could be used as a new target for AKI therapy and reduce the mortality caused by the complication.

Indexed as

Acute Kidney InjuryAcute Lung InjuryReperfusion InjuryAnimalsApoptosisAutophagyBeclin-1BiomarkersCaspase 3CytokinesKidneyMaleProto-Oncogene Proteins c-bcl-2RatsRats, Sprague-DawleySirolimusBeclin-1BiomarkersCaspase 3CytokinesProto-Oncogene Proteins c-bcl-2Sirolimusacute kidney injuryacute lung injuryapoptosisAutophagyischemic reperfusion injury

Identifiers

PMID36259464
PMCPMC9586646
OpenAlexW4306780807

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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.