Evidence map›Paper›PMID 31833196›Full record

ArticleAging cell2020

Progerin in muscle leads to thermogenic and metabolic defects via impaired calcium homeostasis.

Wan-Ping Wang, Jing-Ya Wang, Wen-Hsin Lin, Cheng-Heng Kao, Ming-Chun Hung, Yuan-Chi Teng, Ting-Fen Tsai, Ya-Hui Chi

Open access · goldAbstract read
In one paragraph

Article in Aging cell, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
0.9field-weighted citation impact, top 26% 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

16 citing papers in PubMed, 21 citations in OpenAlex.

  1. Article
  2. Effects of electromyostimulation on sarcolipin and CaBiochemistry and biophysics reports · 2026
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  12. Strain-specific differences in muscle CaThe Journal of experimental biology · 2021
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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

8 authors at 3 institutions in 1 country.

Wan-Ping WangInstitute of Biotechnology and Pharmaceutical Research, National Health Research Institutes, Zhunan, Taiwan.
Jing-Ya WangInstitute of Biotechnology and Pharmaceutical Research, National Health Research Institutes, Zhunan, Taiwan.
Wen-Hsin LinInstitute of Biotechnology and Pharmaceutical Research, National Health Research Institutes, Zhunan, Taiwan.
Cheng-Heng KaoCenter of General Education, Chang Gung University, Taoyuan, Taiwan.
Ming-Chun HungInstitute of Biotechnology and Pharmaceutical Research, National Health Research Institutes, Zhunan, Taiwan.
Yuan-Chi TengDepartment of Life Sciences and Institute of Genome Sciences, National Yang-Ming University, Taipei, Taiwan.
Ting-Fen TsaiInstitute of Biotechnology and Pharmaceutical Research, National Health Research Institutes, Zhunan, Taiwan.
Ya-Hui ChiInstitute of Biotechnology and Pharmaceutical Research, National Health Research Institutes, Zhunan, Taiwan.ORCID 0000-0002-9216-0938
National Health Research Institutes · TWNational Yang Ming Chiao Tung University · TWChang Gung University · TW

Funding

Ministry of Science and Technology 104-2633-B-400-001Ministry of Science and Technology 105-2320-B-400-020Ministry of Science and Technology 105-2633-B-400-001Ministry of Science and Technology 107-2319-B-001-002National Taiwan University
6 · The paper itself

Abstract

Mutations in lamin A (LMNA) are responsible for a variety of human dystrophic and metabolic diseases. Here, we created a mouse model in which progerin, the lamin A mutant protein that causes Hutchinson-Gilford progeria syndrome (HGPS), can be inducibly overexpressed. Muscle-specific overexpression of progerin was sufficient to induce muscular dystrophy and alter whole-body energy expenditure, leading to premature death. Intriguingly, sarcolipin (Sln), an endoplasmic reticulum (ER)-associated protein involved in heat production, is upregulated in progerin-expressing and Lmna knockout (Lmna

Indexed as

AnimalsCalciumCalnexinCell NucleusDisease Models, AnimalEndoplasmic ReticulumEndoplasmic Reticulum StressLamin Type AMiceMice, KnockoutMicroscopy, Electron, TransmissionMuscle ProteinsMuscle, SkeletalMuscular DystrophiesMutationMyoblastsCalciumCalnexinLamin Type AMuscle ProteinsORAI1 ProteinOrai1 protein, mouseProteolipidssarcolipinStim1 protein, mouseStromal Interaction Molecule 1agingcalcium homeostasislamin Amuscular dystrophyprogeria

Identifiers

PMID31833196
PMCPMC6996945
OpenAlexW2994939802

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.