Evidence map›Paper›PMID 31696221›Full record

ArticleBioscience reports2019

Malignant fibrous histiocytoma amplified sequence 1 alleviates inflammation and renal fibrosis in diabetic nephropathy by inhibiting TLR4.

Huan Lian, Yi Cheng, Xiaoyan Wu

Open access · goldAbstract read
In one paragraph

Article in Bioscience reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed, 1 pooled it
0.4field-weighted citation impact, top 32% 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

3 citing papers in PubMed, 1 synthesis or guideline pooled it, 4 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. 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

3 authors at 2 institutions in 1 country.

Huan LianDepartment of Nephrology, Zhongnan Hospital of Wuhan University, Wuhan 430071, P.R. China.
Yi ChengTongji Hospital, Tongji Medical College of Huazhong University of Science and Technology, Wuhan 430030, P.R. China.
Xiaoyan WuDepartment of Nephrology, Zhongnan Hospital of Wuhan University, Wuhan 430071, P.R. China.
Wuhan University · CNTongji Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundDiabetic nephropathy (DN) is the most common complication of diabetes mellitus (DM). The signal pathway and molecular mechanism of renal fibrosis are not fully understood. In the present study, we aimed to explore the function of malignant fibrous histiocytoma amplified sequence 1 (MFHAS1) in DN.

methodMouse mesangial cells (MMCs) were treated with low glucose (LG) or high glucose (HG). TAK242 or short hairpin TLR4 (shTLR4) were employed to down-regulate Toll-like receptor 4 (TLR4). The effect of MFHAS1 knockdown or overexpression on fibrosis-related factors, inflammatory factors and TLR4 in MMCs were examined after transfecting with short hairpin RNA (shRNA) or MFHAS1 overexpressed plasmid, respectively. The expression levels of MFHAS1, inflammatory factors, fibrosis factors and TLR4 in db/db or streptozotocin (STZ) mice tissues and MMCs were examined by quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot. The effect of MFHAS1 overexpression in vivo was also evaluated.

resultsThe expression of MFHAS1 in db/db or STZ mice and HG-treated MMCs were significantly increased compared with normal control mice and LG-treated MMCs. Overexpression of MFHAS1 inhibited the expression of inflammatory and fibrotic factors, while knockdown of MFHAS1 promoted them. MFHAS1 suppressed the activation of TLR4 pathway via inhibiting the expression of TLR4, and then alleviating inflammation and fibrosis in DN. MFHAS1 overexpression in vivo improved the symptoms of STZ-induced DN mice.

conclusionThe current study demonstrated that MFHAS1 relieved inflammation and renal fibrosis in DN mice via inhibiting TLR4. The results revealed that the MFHAS1 may be a molecular target in DN therapy.

Indexed as

AnimalsCells, CulturedDiabetes Mellitus, ExperimentalDiabetic NephropathiesDNA-Binding ProteinsFibrosisHistiocytoma, Malignant FibrousInflammationKidneyMaleMesangial CellsMiceMice, Inbred C57BLSignal TransductionStreptozocinToll-Like Receptor 4DNA-Binding ProteinsStreptozocinTlr4 protein, mouseToll-Like Receptor 4animal modelDiabetic nephropathyMFHAS1renal fibrosisTLR4

Identifiers

PMID31696221
PMCPMC6851511
OpenAlexW2981030134

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.