Evidence map›Paper›PMID 38634132›Full record

ArticleAmerican journal of physiology. Renal physiology2024

JAK inhibition during the early phase of SARS-CoV-2 infection worsens kidney injury by suppressing endogenous antiviral activity in mice.

Hibiki Sakai, Hiroyasu Kamuro, Nagisa Tokunoh, Takeshi Izawa, Shigeyuki Tamiya, Ayaha Yamamoto, Shota Tanaka, Daisuke Okuzaki, Chikako Ono, Yoshiharu Matsuura and 4 more

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Renal physiology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
1.6field-weighted citation impact, top 19% 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

2 citing papers in PubMed, 4 citations in OpenAlex.

  1. Article
  2. 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

14 authors at 5 institutions in 1 country.

Hibiki SakaiLaboratory of Clinical Science and Biomedicine, Graduate School of Pharmaceutical Sciences, Osaka University, Osaka, Japan.
Hiroyasu KamuroLaboratory of Clinical Science and Biomedicine, Graduate School of Pharmaceutical Sciences, Osaka University, Osaka, Japan.
Nagisa TokunohVaccine Creation Group, BIKEN Innovative Vaccine Research Alliance Laboratories, Research Institute for Microbial Diseases, Osaka University, Osaka, Japan.
Takeshi IzawaLaboratory of Veterinary Pathology, Osaka Metropolitan University Graduate School of Veterinary Science, Osaka, Japan.
Shigeyuki TamiyaVaccine Creation Group, BIKEN Innovative Vaccine Research Alliance Laboratories, Research Institute for Microbial Diseases, Osaka University, Osaka, Japan.
Ayaha YamamotoLaboratory of Clinical Science and Biomedicine, Graduate School of Pharmaceutical Sciences, Osaka University, Osaka, Japan.
Shota TanakaLaboratory of Clinical Science and Biomedicine, Graduate School of Pharmaceutical Sciences, Osaka University, Osaka, Japan.ORCID 0000-0002-3053-6928
Daisuke OkuzakiGenome Information Research Center, Research Institute for Microbial Diseases, Osaka University, Osaka, Japan.ORCID 0000-0002-4552-783X
Chikako OnoLaboratory of Virus Control, Research Institute for Microbial Diseases, Osaka University, Osaka, Japan.
Yoshiharu MatsuuraLaboratory of Virus Control, Research Institute for Microbial Diseases, Osaka University, Osaka, Japan.
Yoshiaki OkadaLaboratory of Clinical Science and Biomedicine, Graduate School of Pharmaceutical Sciences, Osaka University, Osaka, Japan.ORCID 0000-0002-2962-244X
Yasuo YoshiokaVaccine Creation Group, BIKEN Innovative Vaccine Research Alliance Laboratories, Research Institute for Microbial Diseases, Osaka University, Osaka, Japan.
Yasushi FujioLaboratory of Clinical Science and Biomedicine, Graduate School of Pharmaceutical Sciences, Osaka University, Osaka, Japan.ORCID 0000-0003-0828-2930
Masanori ObanaLaboratory of Clinical Science and Biomedicine, Graduate School of Pharmaceutical Sciences, Osaka University, Osaka, Japan.ORCID 0000-0002-3209-2208
Osaka International Cancer Institute · JPThe University of Osaka · JPKyoto Biken Laboratories (Japan) · JPOsaka Metropolitan University · JPWakayama Medical University · JP

Funding

Hoansha Foundation ( )Japan Agency for Medical Research and Development (AMED) JP23ama121052,JP23ama121054Japanese Association of Dialysis Physicians (JAPD)Mochida Memorial Foundation for Medical and Pharmaceutical Research ( )Nippon Foundation
6 · The paper itself

Abstract

Coronavirus disease 2019 (COVID-19) induces respiratory dysfunction as well as kidney injury. Although the kidney is considered a target organ of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and affected by the COVID-19-induced cytokine storm, the mechanisms of renal reaction in SARS-CoV-2 infection are unknown. In this study, a murine COVID-19 model was induced by nasal infection with mouse-adapted SARS-CoV-2 (MA10). MA10 infection induced body weight loss along with lung inflammation in mice 4 days after infection. Serum creatinine levels and the urinary albumin/creatinine ratio increased on

Indexed as

COVID-19Janus Kinase InhibitorsPurinesPyrazolesSARS-CoV-2SulfonamidesAcute Kidney InjuryAnimalsAntiviral AgentsAzetidinesCOVID-19 Drug TreatmentDisease Models, AnimalJanus KinasesKidneyMaleMiceAntiviral AgentsAzetidinesbaricitinibJanus Kinase InhibitorsJanus KinasesPurinesPyrazolesSulfonamidesantiviral activitybaricitinibJAKkidney injurySARS-CoV-2

Identifiers

PMID38634132
PMCPMC11381010
OpenAlexW4394918457

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.