Evidence map›Paper›PMID 25973045›Full record

ArticleInternational journal of clinical and experimental pathology2015

Local bone interaction between renin-angiotensin system and kallikrein-kinin system in diabetic rat.

Yong Li, Guang-Si Shen, Chen Yu, Guang-Fei Li, Jun-Kang Shen, You-Jia Xu, Jian-Ping Gong

Open access · greenAbstract read
In one paragraph

Article in International journal of clinical and experimental pathology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.7field-weighted citation impact, top 26% 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

4 citing papers in PubMed, 6 citations in OpenAlex.

  1. Article
  2. Article
  3. Renin inhibitor aliskiren exerts beneficial effect on trabecular bone by regulating skeletal renin-angiotensin system and kallikrein-kinin system in ovariectomized mice.Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA · 2016
    Article
  4. Article
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

7 authors at 1 institution in 1 country.

Yong LiDepartment of Radiology, The Second Affiliated Hospital of Soochow University 1055 Sanxiang Road, Suzhou, China.
Guang-Si ShenDepartment of Orthopaedics, The Second Affiliated Hospital of Soochow University 1055 Sanxiang Road, Suzhou, China.
Chen YuDepartment of Orthopaedics, The Second Affiliated Hospital of Soochow University 1055 Sanxiang Road, Suzhou, China.
Guang-Fei LiDepartment of Orthopaedics, The Second Affiliated Hospital of Soochow University 1055 Sanxiang Road, Suzhou, China.
Jun-Kang ShenDepartment of Radiology, The Second Affiliated Hospital of Soochow University 1055 Sanxiang Road, Suzhou, China.
You-Jia XuDepartment of Orthopaedics, The Second Affiliated Hospital of Soochow University 1055 Sanxiang Road, Suzhou, China.
Jian-Ping GongDepartment of Radiology, The Second Affiliated Hospital of Soochow University 1055 Sanxiang Road, Suzhou, China.
Soochow University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveThis study was performed to investigate bone deteriorations and the involvement of skeletal renin-angiotensin system (RAS) and kallikrein-kinin system (KKS) of male rat in response to the hyperglycemia.

methodsThe biomarkers in serum and urine were measured by ELISA kit, and tibias were taken for the measurement on gene, protein expression and histological analysis, femurs were taken for the measurement on biomechanical parameters and micro-CT.

resultsThe DM1 showed the decreased level of osteocalcin, testosterone and FGF-23, and the increased level of serum CTX as compared to those of vehicle group. The H&E staining showed remarkable bone deteriorations, including increased disconnections and separation of trabecular bone among growth plate and joint cartilage in DM1 group. Biomechanically, the maximum load, maximum stress, and strain parameter of DM1 group was significantly lower than control group. Type 1 diabetic mice displayed bone loss shown the reduction of bone volume/total volume, trabecular number, trabecular thickness and bone mineral density. The STZ injection significantly up-regulated mRNA expression of AT1R, AGT, renin, renin-receptor, and ACE, and the expression of AT2R, B1R and B2R were down-regulated in tibia of rat in hyperglycemia group. The protein expression of renin, ACE and Ang II were significantly up-regulated, and AT2R, B1R and B2R were down-regulated in DM1 group.

conclusionsThe treatment of hyperglycemia was detrimental to bone as compared to the vehicle group, and the underlying mechanism was mediated, at least partially, through down-regulation of KSS activity and up-regulation of RAS activity in local bone.

Indexed as

AnimalsBlotting, WesternBone and BonesDiabetes Mellitus, ExperimentalDiabetes Mellitus, Type 1Enzyme-Linked Immunosorbent AssayFibroblast Growth Factor-23Kallikrein-Kinin SystemMaleRatsRats, Sprague-DawleyReal-Time Polymerase Chain ReactionRenin-Angiotensin SystemFibroblast Growth Factor-23bonehyperglycemiakallikrein-kinin systemRenin-angiotensin system

Identifiers

PMID25973045
PMCPMC4396287
OpenAlexW2406310851

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.