Evidence map›Paper›PMID 29207166›Full record

ArticleInternational journal of molecular medicine2018

Pentosan polysulfate ameliorates apoptosis and inflammation by suppressing activation of the p38 MAPK pathway in high glucose‑treated HK‑2 cells.

Ping Chen, Yang Yuan, Tianying Zhang, Bo Xu, Qing Gao, Tianjun Guan

Open access · hybridAbstract read
In one paragraph

Article in International journal of molecular medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.1field-weighted citation impact, top 24% 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

17 citing papers in PubMed, 28 citations in OpenAlex.

  1. Article
  2. Recent advances in the role of gasotransmitters in necroptosis.Apoptosis : an international journal on programmed cell death · 2025
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  5. Pathomechanisms of Diabetic Kidney Disease.Journal of clinical medicine · 2023
    Review
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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

6 authors at 2 institutions in 1 country.

Ping ChenDepartment of Nephrology, Ningbo First Hospital, Ningbo, Zhejiang 315010, P.R. China.
Yang YuanDepartment of Nephrology, Zhongshan Hospital, Xiamen University, Xiamen, Fujian 361004, P.R. China.
Tianying ZhangDepartment of Nephrology, Zhongshan Hospital, Xiamen University, Xiamen, Fujian 361004, P.R. China.
Bo XuDepartment of Nephrology, Zhongshan Hospital, Xiamen University, Xiamen, Fujian 361004, P.R. China.
Qing GaoDepartment of Nephrology, Zhongshan Hospital, Xiamen University, Xiamen, Fujian 361004, P.R. China.
Tianjun GuanDepartment of Nephrology, Zhongshan Hospital, Xiamen University, Xiamen, Fujian 361004, P.R. China.
Zhongshan Hospital of Xiamen University · CNNingbo First Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The apoptosis of tubular epithelial cells in diabetic nephropathy (DN) is commonly observed in human renal biopsies. Inflammation plays a key role in DN, and pentosan polysulfate (PPS) has been shown to largely attenuate the inflammation of nephropathy in aging diabetic mice. p38 mitogen‑activated protein kinase (p38 MAPK) plays a crucial role in tissue inflammation and cell apoptosis, and it is activated by hyperglycemia. In the present study, high glucose (HG)‑treated human renal proximal tubular epithelial cells (HK‑2) were used to examine the protective effects of PPS against HG‑stimulated apoptosis and inflammation. The results of the study revealed that PPS markedly suppressed the HG‑induced reduction in cell viability. Incubation of HK‑2 cells with HG activated the p38 MAPK pathway and, subsequently, as confirmed by western blot analysis and flow cytometry, increased cell apoptosis, which was blocked by PPS. In addition, PPS treatment significantly inhibited HG‑stimulated p38 MAPK and nuclear factor‑κB activation, and reduced the production of pro‑inflammatory cytokines, such as tumor necrosis factor‑α, interleukin (IL)‑1β and IL‑6. In conclusion, PPS ameliorates p38 MAPK‑mediated renal cell apoptosis and inflammation. The anti‑apoptotic actions and anti‑inflammatory effects of PPS prompt further investigation of this compound as a promising therapeutic agent against DN.

Indexed as

AnimalsApoptosisCell SurvivalDiabetic NephropathiesDisease Models, AnimalGlucoseHumansInflammationKidney Tubules, ProximalMiceMice, Inbred NODNF-kappa Bp38 Mitogen-Activated Protein KinasesPentosan Sulfuric PolyesterSignal TransductionGlucoseNF-kappa Bp38 Mitogen-Activated Protein KinasesPentosan Sulfuric Polyester

Identifiers

PMID29207166
PMCPMC5752165
OpenAlexW2770619166

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.