Evidence map›Paper›PMID 33244034›Full record

ArticleScientific reports2020

Systemic and sustained thioredoxin analogue prevents acute kidney injury and its-associated distant organ damage in renal ischemia reperfusion injury mice.

Kento Nishida, Hiroshi Watanabe, Masako Miyahisa, Yuto Hiramoto, Hiroto Nosaki, Rui Fujimura, Hitoshi Maeda, Masaki Otagiri, Toru Maruyama

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

10 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

9 authors at 2 institutions in 1 country.

Kento NishidaDepartment of Biopharmaceutics, Graduate School of Pharmaceutical Sciences, Kumamoto University, 5-1, Oe-honmachi, Chuo-ku, Kumamoto, 862-0973, Japan.
Hiroshi WatanabeDepartment of Biopharmaceutics, Graduate School of Pharmaceutical Sciences, Kumamoto University, 5-1, Oe-honmachi, Chuo-ku, Kumamoto, 862-0973, Japan. hnabe@kumamoto-u.ac.jp.
Masako MiyahisaDepartment of Biopharmaceutics, Graduate School of Pharmaceutical Sciences, Kumamoto University, 5-1, Oe-honmachi, Chuo-ku, Kumamoto, 862-0973, Japan.
Yuto HiramotoDepartment of Biopharmaceutics, Graduate School of Pharmaceutical Sciences, Kumamoto University, 5-1, Oe-honmachi, Chuo-ku, Kumamoto, 862-0973, Japan.
Hiroto NosakiDepartment of Biopharmaceutics, Graduate School of Pharmaceutical Sciences, Kumamoto University, 5-1, Oe-honmachi, Chuo-ku, Kumamoto, 862-0973, Japan.
Rui FujimuraDepartment of Biopharmaceutics, Graduate School of Pharmaceutical Sciences, Kumamoto University, 5-1, Oe-honmachi, Chuo-ku, Kumamoto, 862-0973, Japan.
Hitoshi MaedaDepartment of Biopharmaceutics, Graduate School of Pharmaceutical Sciences, Kumamoto University, 5-1, Oe-honmachi, Chuo-ku, Kumamoto, 862-0973, Japan.
Masaki OtagiriFaculty of Pharmaceutical Sciences, Sojo University, 4-22-1 Ikeda, Kumamoto, 860-0082, Japan.
Toru MaruyamaDepartment of Biopharmaceutics, Graduate School of Pharmaceutical Sciences, Kumamoto University, 5-1, Oe-honmachi, Chuo-ku, Kumamoto, 862-0973, Japan. tomaru@gpo.kumamoto-u.ac.jp.
Kumamoto University · JPSojo University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The mortality of patients with acute kidney injury (AKI) remains high due to AKI associated-lung injury. An effective strategy for preventing both AKI and AKI-associated lung injury is urgently needed. Thioredoxin-1 (Trx) is a redox-active protein that possesses anti-oxidative, anti-apoptotic and anti-inflammatory properties including modulation of macrophage migration inhibitory factor (MIF), but its short half-life limits its clinical application. Therefore, we examined the preventive effect of a long-acting Trx, which is a fusion protein of albumin and Trx (HSA-Trx), against AKI and AKI-associated lung injury. Recombinant HSA-Trx was expressed using a Pichia expression system. AKI-induced lung injury mice were generated by bilateral renal ischemia reperfusion injury (IRI). HSA-Trx administration attenuated renal IRI and its-associated lung injury. Both renal and pulmonary oxidative stress were suppressed by HSA-Trx. Moreover, HSA-Trx inhibited elevations of plasma IL-6 and TNF-α level, and suppressed IL-6-CXCL1/2-mediated neutrophil infiltration into lung and TNF-α-mediated pulmonary apoptosis. Additionally, HSA-Trx suppressed renal IRI-induced MIF expression in kidney and lung. Administration of HSA-Trx resulted in a significant increase in the survival rate of renal IRI mice. Collectively, HSA-Trx could have therapeutic utility in preventing both AKI and AKI-associated lung injury as a consequence of its systemic and sustained multiple biological action.

Indexed as

Acute Kidney InjuryAcute Lung InjuryAnimalsAnti-Inflammatory AgentsAntioxidantsApoptosisDelayed-Action PreparationsDisease Models, AnimalInterleukin-6KidneyLungMacrophage Migration-Inhibitory FactorsMaleMiceMice, Inbred C57BLOxidation-ReductionAnti-Inflammatory AgentsAntioxidantsDelayed-Action PreparationsInterleukin-6Macrophage Migration-Inhibitory FactorsReactive Oxygen SpeciesSerum AlbuminThioredoxinsTumor Necrosis Factor-alpha

Identifiers

PMID33244034
PMCPMC7691343
OpenAlexW3109884468

What OpenQuestion holds

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LicenceCC BY
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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.