Evidence map›Paper›PMID 37353518›Full record

ArticleNature communications2023

Mitochondrial matrix protein LETMD1 maintains thermogenic capacity of brown adipose tissue in male mice.

Anna Park, Kwang-Eun Kim, Isaac Park, Sang Heon Lee, Kun-Young Park, Minkyo Jung, Xiaoxu Li, Maroun Bou Sleiman, Su Jeong Lee, Dae-Soo Kim and 13 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

14 citing papers in PubMed, 16 citations in OpenAlex.

  1. Article
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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

23 authors at 8 institutions in 3 countries.

Anna Park *Metabolic Regulation Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Daejeon, 34141, Republic of Korea.
Kwang-Eun Kim *Graduate School of Medical Science and Engineering, KAIST, Daejeon, 34141, Republic of Korea.
Isaac ParkDepartment of Chemistry, Seoul National University, Seoul, 08826, Republic of Korea.
Sang Heon LeeGraduate School of Medical Science and Engineering, KAIST, Daejeon, 34141, Republic of Korea.
Kun-Young ParkGraduate School of Medical Science and Engineering, KAIST, Daejeon, 34141, Republic of Korea.ORCID 0000-0003-0425-3286
Minkyo JungNeural Circuit Research Group, Korea Brain Research Institute, Daegu, 41068, Republic of Korea.
Xiaoxu LiLaboratory of Integrative Systems Physiology, École polytechnique fédérale de Lausanne (EPFL), CH-1015, Lausanne, Switzerland.
Maroun Bou SleimanLaboratory of Integrative Systems Physiology, École polytechnique fédérale de Lausanne (EPFL), CH-1015, Lausanne, Switzerland.ORCID 0000-0002-1375-7577
Su Jeong LeeMetabolic Regulation Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Daejeon, 34141, Republic of Korea.
Dae-Soo KimDepartment of Functional Genomics, KRIBB School of Bioscience, Korea University of Science and Technology (UST), Daejeon, 34141, Republic of Korea.ORCID 0000-0002-4999-1613
Jaehoon KimDepartment of Biological Sciences, KAIST, Daejeon, 34141, Republic of Korea.
Dae-Sik LimNational Creative Research Center for Cell Plasticity, KAIST Stem Cell Center, Department of Biological Sciences, KAIST, Daejeon, 34141, Republic of Korea.ORCID 0000-0003-2356-7555
Eui-Jeon WooDepartment of Functional Genomics, KRIBB School of Bioscience, Korea University of Science and Technology (UST), Daejeon, 34141, Republic of Korea.ORCID 0000-0001-6983-0270
Eun Woo LeeMetabolic Regulation Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Daejeon, 34141, Republic of Korea.ORCID 0000-0002-5156-0003
Baek Soo HanDepartment of Functional Genomics, KRIBB School of Bioscience, Korea University of Science and Technology (UST), Daejeon, 34141, Republic of Korea.
Kyoung-Jin OhMetabolic Regulation Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Daejeon, 34141, Republic of Korea.ORCID 0000-0002-2224-7202
Sang Chul LeeMetabolic Regulation Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Daejeon, 34141, Republic of Korea.
Johan AuwerxLaboratory of Integrative Systems Physiology, École polytechnique fédérale de Lausanne (EPFL), CH-1015, Lausanne, Switzerland.ORCID 0000-0002-5065-5393
Ji Young MunNeural Circuit Research Group, Korea Brain Research Institute, Daegu, 41068, Republic of Korea.
Hyun-Woo RheeDepartment of Chemistry, Seoul National University, Seoul, 08826, Republic of Korea.ORCID 0000-0002-3817-3455
Won Kon KimMetabolic Regulation Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Daejeon, 34141, Republic of Korea. wkkim@kribb.re.kr.ORCID 0000-0002-1289-0333
Kwang-Hee BaeMetabolic Regulation Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Daejeon, 34141, Republic of Korea. khbae@kribb.re.kr.ORCID 0000-0002-5868-2556
Jae Myoung SuhGraduate School of Medical Science and Engineering, KAIST, Daejeon, 34141, Republic of Korea. jmsuh@kaist.ac.kr.ORCID 0000-0001-8097-4662
Korea Advanced Institute of Science and Technology · KRKorea Research Institute of Bioscience and Biotechnology · KRÉcole Polytechnique Fédérale de Lausanne · CHSeoul National University · KRKorea Brain Research Institute · KRMarine Biodiversity Institute of Korea · KRSTR Biotech (South Korea) · KRUniversity of California, Irvine · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Brown adipose tissue (BAT) has abundant mitochondria with the unique capability of generating heat via uncoupled respiration. Mitochondrial uncoupling protein 1 (UCP1) is activated in BAT during cold stress and dissipates mitochondrial proton motive force generated by the electron transport chain to generate heat. However, other mitochondrial factors required for brown adipocyte respiration and thermogenesis under cold stress are largely unknown. Here, we show LETM1 domain-containing protein 1 (LETMD1) is a BAT-enriched and cold-induced protein required for cold-stimulated respiration and thermogenesis of BAT. Proximity labeling studies reveal that LETMD1 is a mitochondrial matrix protein. Letmd1 knockout male mice display aberrant BAT mitochondria and fail to carry out adaptive thermogenesis under cold stress. Letmd1 knockout BAT is deficient in oxidative phosphorylation (OXPHOS) complex proteins and has impaired mitochondrial respiration. In addition, BAT-specific Letmd1 deficient mice exhibit phenotypes identical to those observed in Letmd1 knockout mice. Collectively, we demonstrate that the BAT-enriched mitochondrial matrix protein LETMD1 plays a tissue-autonomous role that is essential for BAT mitochondrial function and thermogenesis.

Indexed as

Adipose Tissue, BrownMitochondrial ProteinsThermogenesisAdipocytes, BrownAnimalsMaleMiceMice, KnockoutMitochondriaUncoupling Protein 1Mitochondrial ProteinsUncoupling Protein 1

Identifiers

PMID37353518
PMCPMC10290150
OpenAlexW4381739374

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.