Evidence map›Paper›PMID 25826393›Full record

ArticlePloS one2015

Pik3ip1 modulates cardiac hypertrophy by inhibiting PI3K pathway.

Hong Ki Song, Jiyeon Kim, Jong Sub Lee, Kyoung Jin Nho, Hae Chang Jeong, Jihwa Kim, Youngkeun Ahn, Woo Jin Park, Do Han Kim

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

24 citing papers in PubMed, 41 citations in OpenAlex.

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  20. Expression of PIK3IP1 in the murine uterus during early pregnancy.Biochemical and biophysical research communications · 2018
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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.

Hong Ki SongSchool of Life Sciences and Systems Biology Research Center, Gwangju Institute of Science and Technology (GIST), Gwangju, Republic of Korea.
Jiyeon KimSchool of Life Sciences and Systems Biology Research Center, Gwangju Institute of Science and Technology (GIST), Gwangju, Republic of Korea.
Jong Sub LeeSchool of Life Sciences and Systems Biology Research Center, Gwangju Institute of Science and Technology (GIST), Gwangju, Republic of Korea.
Kyoung Jin NhoSchool of Life Sciences and Systems Biology Research Center, Gwangju Institute of Science and Technology (GIST), Gwangju, Republic of Korea.
Hae Chang JeongDepartment of Cardiology, Chonnam National University Hospital, Gwangju, Republic of Korea.
Jihwa KimSchool of Life Sciences and Systems Biology Research Center, Gwangju Institute of Science and Technology (GIST), Gwangju, Republic of Korea.
Youngkeun AhnDepartment of Cardiology, Chonnam National University Hospital, Gwangju, Republic of Korea.
Woo Jin ParkSchool of Life Sciences and Systems Biology Research Center, Gwangju Institute of Science and Technology (GIST), Gwangju, Republic of Korea.
Do Han KimSchool of Life Sciences and Systems Biology Research Center, Gwangju Institute of Science and Technology (GIST), Gwangju, Republic of Korea.
Gwangju Institute of Science and Technology · KRChonnam National University Hospital · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cardiac hypertrophy is an adaptive response to various physiological and pathological stimuli. Phosphoinositide-3 kinase (PI3K) is a highly conserved lipid kinase involved in physiological cardiac hypertrophy (PHH). PI3K interacting protein1 (Pik3ip1) shares homology with the p85 regulatory subunit of PI3K and is known to interact with the p110 catalytic subunit of PI3K, leading to attenuation of PI3K activity in liver and immune cells. However, the role of Pik3ip1 in the heart remains unknown. In the present study, the effects of Pik3ip1 on cardiac hypertrophy were examined. We found that the expression level of Pik3ip1 was markedly higher in cardiomyocytes than in fibroblasts. The interaction of Pik3ip1 with the p110a subunit of PI3K in the heart was identified by immunoprecipitation using neonatal rat cardiomyocytes (NRCM). Approximately 35% knockdown of Pik3ip1 was sufficient to induce myocardial hypertrophy. Pik3ip1 deficiency was shown to lead to activation of PI3K/protein kinase B (AKT)/ mammalian target of rapamycin (mTOR) signaling pathway, increasing protein synthesis and cell size. However, adenovirus-mediated overexpression of Pik3ip1 attenuated PI3K-mediated cardiac hypertrophy. Pik3ip1 was upregulated by PHH due to swimming training, but not by pathological cardiac hypertrophy (PAH) due to pressure-overload, suggesting that Pik3ip1 plays a compensatory negative role for PHH. Collectively, our results elucidate the mechanisms for the roles of Pik3ip1 in PI3K/AKT signaling pathway.

Indexed as

Phosphoinositide-3 Kinase InhibitorsAnimalsAnimals, NewbornCardiomegalyCarrier ProteinsCells, CulturedClass I Phosphatidylinositol 3-KinasesGene SilencingIntracellular Signaling Peptides and ProteinsMaleMembrane ProteinsMiceMice, Inbred C57BLMyocytes, CardiacPhysical Conditioning, AnimalProtein Binding1-phosphatidylinositol 3-kinase p110 subunit, mouseCarrier ProteinsClass I Phosphatidylinositol 3-KinasesIntracellular Signaling Peptides and ProteinsMembrane ProteinsPhosphoinositide-3 Kinase InhibitorsPik3ip1 protein, mouseProto-Oncogene Proteins c-aktRNA, Small Interfering

Identifiers

PMID25826393
PMCPMC4380398
OpenAlexW2058370372

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.