Evidence map›Paper›PMID 34991802›Full record

ArticleKidney international2022

Therapeutic potential of Beclin1 for transition from AKI to CKD: autophagy-dependent and autophagy-independent functions.

Satoshi Minami, Shuhei Nakamura

Abstract readComment
PubMed Publisher
In one paragraph

Article in Kidney international, 2022. 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
2.0field-weighted citation impact, top 14% 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, 14 citations in OpenAlex.

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  8. Roles of NADInternational journal of molecular sciences · 2022
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Satoshi MinamiDepartment of Genetics, Graduate School of Medicine, Osaka University, Suita, Osaka, Japan.
Shuhei NakamuraDepartment of Genetics, Graduate School of Medicine, Osaka University, Suita, Osaka, Japan; Department of Intracellular Membrane Dynamics, Graduate School of Frontier Biosciences, Osaka University, Suita, Osaka, Japan; Institute for Advanced Co-Creation Studies, Osaka University, Suita, Osaka, Japan. Electronic address: shuhei.nakamura@fbs.osaka-u.ac.jp.
Osaka University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acute kidney injury (AKI) increases the risk of chronic kidney disease (CKD), but the mechanisms of CKD development after AKI remain unclear. Recent studies have elucidated that autophagy protects against AKI, but the role of autophagy during the AKI-to-CKD transition is controversial. Beclin1 is a key molecule for autophagy as well as endocytosis and phagocytosis. Shi et al. demonstrate that Beclin1 activates autophagy and is a promising therapeutic target for AKI-to-CKD transition.

Indexed as

Acute Kidney InjuryRenal Insufficiency, ChronicAutophagyBeclin-1HumansBeclin-1

Identifiers

PMID34991802
OpenAlexW4205494378

What OpenQuestion holds

Textmetadata
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.