Evidence map›Paper›PMID 32271168›Full record

ArticleJCI insight2020

Soluble (pro)renin receptor treats metabolic syndrome in mice with diet-induced obesity via interaction with PPARγ.

Fei Wang, Renfei Luo, Chang-Jiang Zou, Shiying Xie, Kexin Peng, Long Zhao, Kevin T Yang, Chuanming Xu, Tianxin Yang

Open access · goldAbstract read
In one paragraph

Article in JCI insight, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.5field-weighted citation impact, top 9% 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

15 citing papers in PubMed, 27 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. The soluble (pro)renin receptor promotes a preeclampsia-like phenotype both in vitro and in vivo.Hypertension research : official journal of the Japanese Society of Hypertension · 2024
    Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. The prorenin receptor and its soluble form contribute to lipid homeostasis.American journal of physiology. Endocrinology and metabolism · 2021
    Article
  14. Article
  15. 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

9 authors at 2 institutions in 2 countries.

Fei WangDepartment of Internal Medicine, University of Utah and Veterans Affairs Medical Center, Salt Lake City, Utah, USA.
Renfei LuoDepartment of Internal Medicine, University of Utah and Veterans Affairs Medical Center, Salt Lake City, Utah, USA.
Chang-Jiang ZouDepartment of Internal Medicine, University of Utah and Veterans Affairs Medical Center, Salt Lake City, Utah, USA.
Shiying XieDepartment of Internal Medicine, University of Utah and Veterans Affairs Medical Center, Salt Lake City, Utah, USA.
Kexin PengDepartment of Internal Medicine, University of Utah and Veterans Affairs Medical Center, Salt Lake City, Utah, USA.
Long ZhaoDepartment of Internal Medicine, University of Utah and Veterans Affairs Medical Center, Salt Lake City, Utah, USA.
Kevin T YangDepartment of Internal Medicine, University of Utah and Veterans Affairs Medical Center, Salt Lake City, Utah, USA.
Chuanming XuDepartment of Internal Medicine, University of Utah and Veterans Affairs Medical Center, Salt Lake City, Utah, USA.
Tianxin YangDepartment of Internal Medicine, University of Utah and Veterans Affairs Medical Center, Salt Lake City, Utah, USA.
University of Utah · USSun Yat-sen University · CN

Funding

Interaction of PGE2 and intrarenal RAS in AngII-induced hypertensionR01DK104072 · NIDDK · UTAH STATE HIGHER EDUCATION SYSTEM--UNIVERSITY OF UTAH · PI YANG, TIANXIN · 2015 to 2025
$3.7M
Role of (pro)renin receptor in aldosterone signaling in the kidneyR01HL139689 · NHLBI · UNIVERSITY OF UTAH · PI YANG, TIANXIN · 2018 to 2021
$2.3M
Interaction of (pro)renin receptor and PPARy in regulation of plasma volumeR01HL135851 · NHLBI · UNIVERSITY OF UTAH · PI YANG, TIANXIN · 2017 to 2021
$2.3M
BLRD VA IK6 BX005223NHLBI NIH HHS R01 HL135851NHLBI NIH HHS R01 HL139689NIDDK NIH HHS R01 DK104072
6 · The paper itself

Abstract

The therapies available for management of obesity and associated conditions are limited, because they are often directed toward an individual component of metabolic syndrome and are associated with adverse effects. Here, we report the multifaceted therapeutic potential of histidine-tagged recombinant soluble (pro)renin receptor (sPRR), termed sPRR-His, in a mouse model of diet-induced obesity (DIO). In the DIO model, 2-week administration of sPRR-His lowered body weight and remarkably improved multiple metabolic parameters in the absence of fluid retention. Conversely, inhibition of endogenous sPRR production by PF429242 induced diabetes and insulin resistance, both of which were reversed by the sPRR-His supplement. At the cellular level, sPRR-His enhanced insulin-induced increases in glucose uptake via upregulation of phosphorylated AKT and protein abundance of glucose transporter 4. Promoter and gene expression analysis revealed PRR as a direct target gene of PPARγ. Adipocyte-specific PPARγ deletion induced severe diabetes and insulin resistance associated with reduced adipose PRR expression and circulating sPRR. The sPRR-His supplement in the null mice nearly normalized blood glucose and insulin levels. Additionally, sPRR-His treatment suppressed DIO-induced renal sodium-glucose cotransporter-2 (SGLT2) expression. Overall, sPRR-His exhibits a therapeutic potential in management of metabolic syndrome via interaction with PPARγ.

Indexed as

AdipocytesAnimalsDietary FatsDisease Models, AnimalMaleMetabolic SyndromeMiceObesityPPAR gammaProrenin ReceptorReceptors, Cell SurfaceDietary FatsPPAR gammaPparg protein, mouseProrenin ReceptorReceptors, Cell SurfaceGlucose metabolismMetabolism

Identifiers

PMID32271168
PMCPMC7205274
OpenAlexW3015694104

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.