Evidence map›Paper›PMID 33398033›Full record

ArticleCommunications biology2021

Activation of mitochondrial TUFM ameliorates metabolic dysregulation through coordinating autophagy induction.

Dasol Kim, Hui-Yun Hwang, Eun Sun Ji, Jin Young Kim, Jong Shin Yoo, Ho Jeong Kwon

Open access · goldAbstract read
In one paragraph

Article in Communications biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
36.6field-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

26 citing papers in PubMed, 332 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

6 authors at 2 institutions in 1 country.

Dasol KimChemical Genomics Global Research Laboratory, Department of Biotechnology, College of Life Science and Biotechnology, Yonsei University, Seoul, 03722, Republic of Korea.ORCID 0000-0003-1314-2940
Hui-Yun HwangChemical Genomics Global Research Laboratory, Department of Biotechnology, College of Life Science and Biotechnology, Yonsei University, Seoul, 03722, Republic of Korea.ORCID 0000-0001-9223-1428
Eun Sun JiBiomedical Omics Group, Korea Basic Science Institute, Ochang, Chungbuk, 28119, Republic of Korea.
Jin Young KimBiomedical Omics Group, Korea Basic Science Institute, Ochang, Chungbuk, 28119, Republic of Korea.
Jong Shin YooBiomedical Omics Group, Korea Basic Science Institute, Ochang, Chungbuk, 28119, Republic of Korea.
Ho Jeong KwonChemical Genomics Global Research Laboratory, Department of Biotechnology, College of Life Science and Biotechnology, Yonsei University, Seoul, 03722, Republic of Korea. kwonhj@yonsei.ac.kr.ORCID 0000-0002-6919-833X
Korea Basic Science Institute · KRYonsei University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Disorders of autophagy, a key regulator of cellular homeostasis, cause a number of human diseases. Due to the role of autophagy in metabolic dysregulation, there is a need to identify autophagy regulators as therapeutic targets. To address this need, we conducted an autophagy phenotype-based screen and identified the natural compound kaempferide (Kaem) as an autophagy enhancer. Kaem promoted autophagy through translocation of transcription factor EB (TFEB) without MTOR perturbation, suggesting it is safe for administration. Moreover, Kaem accelerated lipid droplet degradation in a lysosomal activity-dependent manner in vitro and ameliorated metabolic dysregulation in a diet-induced obesity mouse model. To elucidate the mechanism underlying Kaem's biological activity, the target protein was identified via combined drug affinity responsive target stability and LC-MS/MS analyses. Kaem directly interacted with the mitochondrial elongation factor TUFM, and TUFM absence reversed Kaem-induced autophagy and lipid degradation. Kaem also induced mitochondrial reactive oxygen species (mtROS) to sequentially promote lysosomal Ca

Indexed as

3T3-L1 CellsAdipocytesAnimalsAutophagyAutophagy-Related Protein 12Autophagy-Related Protein 5Basic Helix-Loop-Helix Leucine Zipper Transcription FactorsDrug Evaluation, PreclinicalHeLa CellsHumansKaempferolsLipid MetabolismMetabolic SyndromeMiceMice, Inbred C57BLMitochondrial ProteinsAutophagy-Related Protein 12Autophagy-Related Protein 5Basic Helix-Loop-Helix Leucine Zipper Transcription FactorskaempferideKaempferolsMitochondrial ProteinsPeptide Elongation Factor TuTFEB protein, humanTufm protein, mouse

Identifiers

PMID33398033
PMCPMC7782552
OpenAlexW3119671147

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.