Evidence map›Paper›PMID 27798124›Full record

ArticleJournal of the renin-angiotensin-aldosterone system : JRAAS2016

Cross-talk between AMP-activated protein kinase and renin-angiotensin system in uninephrectomised rats.

Ke-Ke Yang, Yi Sui, Hui-Rong Zhou, Jian Shen, Ning Tan, Yan-Mei Huang, Sha-Sha Li, Yan-Hong Pan, Xiao-Xi Zhang, Hai-Lu Zhao

Open access · hybridAbstract read
In one paragraph

Article in Journal of the renin-angiotensin-aldosterone system : JRAAS, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

6 citing papers in PubMed, 16 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Review
  6. Risk for cancer in living kidney donors and recipients.Journal of cancer research and clinical oncology · 2018
    Review
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.

Ke-Ke YangCenter for Diabetic Systems Medicine, Guilin Medical University, China.
Yi SuiCenter for Diabetic Systems Medicine, Guilin Medical University, China.
Hui-Rong ZhouCenter for Diabetic Systems Medicine, Guilin Medical University, China.
Jian ShenCenter for Diabetic Systems Medicine, Guilin Medical University, China.
Ning TanCentral Laboratory of Core Facilities, Guilin Medical University, China.
Yan-Mei HuangCenter for Diabetic Systems Medicine, Guilin Medical University, China.
Sha-Sha LiCenter for Diabetic Systems Medicine, Guilin Medical University, China.
Yan-Hong PanCenter for Diabetic Systems Medicine, Guilin Medical University, China.
Xiao-Xi ZhangCenter for Diabetic Systems Medicine, Guilin Medical University, China.
Hai-Lu ZhaoCenter for Diabetic Systems Medicine, Guilin Medical University, China zhaohailu9@126.com.
Guilin Medical University · CNAffiliated Hospital of Nantong University · CNSouthern Medical University Shenzhen Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionThe renal renin-angiotensin system (RAS) and the ultrasensitive energy sensor AMP-activated protein kinase (AMPK) have been implicated in normal and aberrant states of the kidney, but interaction between the RAS and AMPK remains unknown.

methodsNinety-six rats were stratified into four groups: sham, uninephrectomised, uninephrectomised rats treated with the angiotensin-converting enzyme inhibitor lisinopril or the angiotensin receptor blocker losartan. Histopathological examination at 9 months post-operation and biochemical measurements at 3, 6 and 9 months were performed for changes in renal structure and function. The expression of AMPK and angiotensin II at 9 months was detected by immunofluorescence microscopy and western blot.

resultsCompared with sham rats, uninephrectomised rats demonstrated progressive glomerulosclerosis, tubular atrophy with cast formation and chronic inflammatory infiltration, in parallel to elevated serum urea, creatinine, urine total protein to creatinine ratio and reduced serum albumin. Overexpression of angiotensin II coexisted with a 85.6% reduction of phosphorylated to total AMPK ratio in the remnant kidney of uninephrectomised rats. RAS blockade by the angiotensin-converting enzyme inhibitor or angiotensin receptor blocker substantially normalised AMPK expression, morphological and functional changes of the remnant kidney.

conclusionsUninephrectomy-induced RAS activation and AMPK inhibition in the remnant kidney could be substantially corrected by RAS blockade, suggesting a cross-talk between AMPK and RAS components in uninephrectomised rats.

Indexed as

NephrectomyRenin-Angiotensin SystemAMP-Activated Protein KinasesAngiotensin IAngiotensin IIAnimalsEnzyme ActivationFluorescent Antibody TechniqueKidneyMaleMicroscopy, ConfocalPhosphorylationRats, Sprague-DawleyAMP-Activated Protein KinasesAngiotensin IAngiotensin IIAMP-activated protein kinaseangiotensin-converting enzyme inhibitorangiotensin receptor blockerrenal impairmentRenin–angiotensin systemuninephrectomy

Identifiers

PMID27798124
PMCPMC5843864
OpenAlexW2544506739

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.