Evidence map›Paper›PMID 29672566›Full record

ArticlePloS one2018

Exogenous pentraxin-3 inhibits the reactive oxygen species-mitochondrial and apoptosis pathway in acute kidney injury.

Hyung Ho Lee, Sook Young Kim, Joon Chae Na, Young Eun Yoon, Woong Kyu Han

Registry-linked trialOpen access · goldAbstract read
In one paragraph

Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT06498336 (Specific miRNA Associated With Endothelial Dysfunction and Mitochondrial Damage in Patients With Septic Acute Kidney Injury), which is not on this map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.0field-weighted citation impact, top 27% 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.

NCT06498336 completednot on this mapstarted 2024, after this paper: background citation

Specific miRNA Associated With Endothelial Dysfunction and Mitochondrial Damage in Patients With Septic Acute Kidney Injury

TypeobservationalSponsorUniversity Hospital OstravaRan2024 to 2026Enrolled211ConditionsSepsis, Acute Kidney Injury, Acute Kidney Injury Due to SepsisArmsLaboratory examination to determine the presence of sepsis, Laboratory examination to determine the presence of sepsis and acute kidney injury, Laboratory examination to determine miRNA and biochemical parameters
3 · Its place in the literature

Who cites it

8 citing papers in PubMed, 19 citations in OpenAlex.

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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

5 authors at 2 institutions in 1 country.

Hyung Ho LeeDepartment of Urology, National Health Insurance Service Ilsan Hospital, Gyeonggi-do, Korea.
Sook Young KimDepartment of Urology, Urological Science Institute, Yonsei University College of Medicine, Seoul, Korea.
Joon Chae NaDepartment of Urology, Urological Science Institute, Yonsei University College of Medicine, Seoul, Korea.
Young Eun YoonDepartment of Urology, Hanyang University College of Medicine, Seoul, Korea.
Woong Kyu HanDepartment of Urology, Urological Science Institute, Yonsei University College of Medicine, Seoul, Korea.ORCID 0000-0002-2527-4046
Yonsei University · KRHanyang University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pentraxin-3 (PTX3) is a long-form member of the pentraxin family of proteins that has been studied in inflammatory diseases and in various organs. We found that PTX3 protects kidney cells during ischemia and proinflammatory acute kidney injury. The aim of this study was to develop an in vitro experimental model of acute kidney injury and to analyze the protective mechanism of exogenous recombinant PTX3. In this study, cells of the HK-2 renal tubular cell line were treated with a calcium ionophore (A23187), which induced injury by increasing intracellular calcium concentrations and inducing calpain activity and the generation of reactive oxygen species. Exposure of cells to PTX3 significantly attenuated these effects. In addition, the activity of caspase-3 and PARP-1 were decreased in ischemic cells exposed to exogenous recombinant PTX3. PTX3 stabilized the mitochondrial membrane potential and suppressed apoptosis, resulting in the protection of renal tubular cells from ischemic injury.

Indexed as

Acute Kidney InjuryApoptosisCell LineCell SurvivalC-Reactive ProteinHumansHypoxiaIschemiaMatrix MetalloproteinasesMitochondriaPentraxinsProtective AgentsReactive Oxygen SpeciesSerum Amyloid P-ComponentC-Reactive ProteinMatrix MetalloproteinasesPentraxinsProtective AgentsReactive Oxygen SpeciesSerum Amyloid P-Component

Identifiers

PMID29672566
PMCPMC5909599
OpenAlexW2800328458

What OpenQuestion holds

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Registered trials

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.