Evidence map›Paper›PMID 33420039›Full record

ArticleNature communications2021

An autophagy enhancer ameliorates diabetes of human IAPP-transgenic mice through clearance of amyloidogenic oligomer.

Jinyoung Kim, Kihyoun Park, Min Jung Kim, Hyejin Lim, Kook Hwan Kim, Sun-Woo Kim, Eun-Seo Lee, Hyongbum Henry Kim, Sung Joo Kim, Kyu Yeon Hur and 5 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed, 1 pooled it
10.0field-weighted citation impact, top 1% 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

40 citing papers in PubMed, 1 synthesis or guideline pooled it, 53 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

15 authors at 4 institutions in 1 country.

Jinyoung KimSeverance Biomedical Science Institute, Yonsei University College of Medicine, Seoul, Korea.ORCID 0000-0002-3810-8549
Kihyoun ParkSeverance Biomedical Science Institute, Yonsei University College of Medicine, Seoul, Korea.
Min Jung KimDepartment of Endocrinology and Metabolism, College of Medicine, The Catholic University of Korea, Seoul, Korea.
Hyejin LimSeverance Biomedical Science Institute, Yonsei University College of Medicine, Seoul, Korea.
Kook Hwan KimSeverance Biomedical Science Institute, Yonsei University College of Medicine, Seoul, Korea.
Sun-Woo KimSeverance Biomedical Science Institute, Yonsei University College of Medicine, Seoul, Korea.
Eun-Seo LeeDepartment of Pharmacology, Yonsei University College of Medicine, Seoul, Korea.
Hyongbum Henry KimDepartment of Pharmacology, Yonsei University College of Medicine, Seoul, Korea.ORCID 0000-0002-4693-738X
Sung Joo KimDepartment of Health Sciences and Technology, Samsung Advanced Institute for Health Science and Technology, Sungkyunkwan University School of Medicine, Seoul, Korea.
Kyu Yeon HurDepartment of Health Sciences and Technology, Samsung Advanced Institute for Health Science and Technology, Sungkyunkwan University School of Medicine, Seoul, Korea.
Jae Hyeon KimDepartment of Health Sciences and Technology, Samsung Advanced Institute for Health Science and Technology, Sungkyunkwan University School of Medicine, Seoul, Korea.
Jin Hee AhnDepartment of Chemistry, Gwangju Institute of Science and Technology, Gwangju, Korea.ORCID 0000-0002-6957-6062
Kun-Ho YoonDepartment of Endocrinology and Metabolism, College of Medicine, The Catholic University of Korea, Seoul, Korea.
Ji-Won KimDepartment of Endocrinology and Metabolism, College of Medicine, The Catholic University of Korea, Seoul, Korea.
Myung-Shik LeeSeverance Biomedical Science Institute, Yonsei University College of Medicine, Seoul, Korea. mslee0923@yuhs.ac.ORCID 0000-0003-3292-1720
Yonsei University · KRCatholic University of Korea · KRGwangju Institute of Science and Technology · KRSamsung (South Korea) · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We have reported that autophagy is crucial for clearance of amyloidogenic human IAPP (hIAPP) oligomer, suggesting that an autophagy enhancer could be a therapeutic modality against human diabetes with amyloid accumulation. Here, we show that a recently identified autophagy enhancer (MSL-7) reduces hIAPP oligomer accumulation in human induced pluripotent stem cell-derived β-cells (hiPSC-β-cells) and diminishes oligomer-mediated apoptosis of β-cells. Protective effects of MSL-7 against hIAPP oligomer accumulation and hIAPP oligomer-mediated β-cell death are significantly reduced in cells with knockout of MiTF/TFE family members such as Tfeb or Tfe3. MSL-7 improves glucose tolerance and β-cell function of hIAPP

Indexed as

AmyloidAmyloidogenic ProteinsAnimalsApoptosisAutophagyBasic Helix-Loop-Helix Leucine Zipper Transcription FactorsDiabetes Mellitus, Type 2Gene Knockout TechniquesHumansInduced Pluripotent Stem CellsInsulin-Secreting CellsIslet Amyloid PolypeptideMacroautophagyMiceMice, TransgenicAmyloidAmyloidogenic ProteinsBasic Helix-Loop-Helix Leucine Zipper Transcription FactorsIslet Amyloid PolypeptideTcfe3 protein, mouseTcfeb protein, mouse

Identifiers

PMID33420039
PMCPMC7794419
OpenAlexW3120735080

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.