Evidence map›Paper›PMID 30831319›Full record

ArticleCellular and molecular gastroenterology and hepatology2019

Defective Phosphatidylglycerol Remodeling Causes Hepatopathy, Linking Mitochondrial Dysfunction to Hepatosteatosis.

Xiaoyang Zhang, Jun Zhang, Haoran Sun, Xueling Liu, Yue Zheng, Dan Xu, Jianing Wang, Dandan Jia, Xianlin Han, Feng Liu and 2 more

Open access · goldAbstract read
In one paragraph

Article in Cellular and molecular gastroenterology and hepatology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
3.4field-weighted citation impact, top 8% 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

34 citing papers in PubMed, 59 citations in OpenAlex.

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  12. Biological mechanism and functional verification of key genes related to major depressive disorder and type 2 diabetes mellitus.Mammalian genome : official journal of the International Mammalian Genome Society · 2025
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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

12 authors at 3 institutions in 2 countries.

Xiaoyang ZhangDepartment of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Nanjing Medical University, Nanjing, China.
Jun ZhangSam and Ann Barshop Institute for Longevity and Aging Studies, Department of Pharmacology, University of Texas Health Science Center at San Antonio, San Antonio, Texas.
Haoran SunDepartment of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Nanjing Medical University, Nanjing, China.
Xueling LiuDepartment of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Nanjing Medical University, Nanjing, China.
Yue ZhengDepartment of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Nanjing Medical University, Nanjing, China.
Dan XuCollege of Veterinary Medicine, South China Agricultural University, Guangzhou, China.
Jianing WangSam and Ann Barshop Institute for Longevity and Aging Studies, Department of Pharmacology, University of Texas Health Science Center at San Antonio, San Antonio, Texas.
Dandan JiaSam and Ann Barshop Institute for Longevity and Aging Studies, Department of Pharmacology, University of Texas Health Science Center at San Antonio, San Antonio, Texas.
Xianlin HanSam and Ann Barshop Institute for Longevity and Aging Studies, Department of Pharmacology, University of Texas Health Science Center at San Antonio, San Antonio, Texas.
Feng LiuSam and Ann Barshop Institute for Longevity and Aging Studies, Department of Pharmacology, University of Texas Health Science Center at San Antonio, San Antonio, Texas.
Jia NieSam and Ann Barshop Institute for Longevity and Aging Studies, Department of Pharmacology, University of Texas Health Science Center at San Antonio, San Antonio, Texas.
Yuguang ShiDepartment of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Nanjing Medical University, Nanjing, China; Sam and Ann Barshop Institute for Longevity and Aging Studies, Department of Pharmacology, University of Texas Health Science Center at San Antonio, San Antonio, Texas. Electronic address: syg@njmu.edu.cn.
The University of Texas Health Science Center at San Antonio · USNanjing Medical University · CNSouth China Agricultural University · CN

Funding

TRANSGENIC COREP30AG013319 · NIA · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI PETER J HORNSBY · 1995 to 2026
$30.6M
San Antonio OAIC - Research Education Component (REC)P30AG044271 · NIA · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI Adam Salmon, Elena Volpi · 2015 to 2026
$14.1M
Regulation of Mitochondrial Dysfunction in Diet-Induced Obesity by ALCAT-1R01DK076685 · NIDDK · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI SHI, YUGUANG · 2008 to 2017
$2.8M
Cellular Senescence in Aging-related Metabolic DiseasesR01AG055747 · NIA · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI SHI, YUGUANG · 2017 to 2021
$1.6M
Regulation of Mitochondrial Biogenesis and Function by DsbA-L in the LiverR01DK114479 · NIDDK · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI FRAZER, ALAN · 2018 to 2021
$1.4M
NIA NIH HHS P30 AG013319NIA NIH HHS P30 AG044271NIA NIH HHS R01 AG055747NIDDK NIH HHS R01 DK076685NIDDK NIH HHS R01 DK114479
6 · The paper itself

Abstract

BACKGROUND &

aimsObesity promotes the development of nonalcoholic fatty liver diseases (NAFLDs), yet not all obese patients develop NAFLD. The underlying causes for this discrepancy remain elusive. LPGAT1 is an acyltransferase that catalyzes the remodeling of phosphatidylglycerol (PG), a mitochondrial phospholipid implicated in various metabolic diseases. Here, we investigated the role of LPGAT1 in regulating the onset of diet-induced obesity and its related hepatosteatosis because polymorphisms of the LPGAT1 gene promoter were strongly associated with susceptibility to obesity in Pima Indians.

methodsMice with whole-body knockout of LPGAT1 were generated to investigate the role of PG remodeling in NAFLD.

resultsLPGAT1 deficiency protected mice from diet-induced obesity, but led to hepatopathy, insulin resistance, and NAFLD as a consequence of oxidative stress, mitochondrial DNA depletion, and mitochondrial dysfunction.

conclusionsThis study identified an unexpected role of PG remodeling in obesity, linking mitochondrial dysfunction to NAFLD.

Indexed as

AcyltransferasesAnimalsCardiolipinsDietEndoplasmic Reticulum StressFatty LiverFemaleHepatocytesInsulinInsulin ResistanceLiver CirrhosisMaleMice, KnockoutMitochondriaNon-alcoholic Fatty Liver DiseaseObesityAcyltransferasesCardiolipinsInsulinPhosphatidylglycerolsCardiolipinLPGAT1MEGDEL SyndromeMitochondrial DysfunctionNAFLD

Identifiers

PMID30831319
PMCPMC6463126
OpenAlexW2920355054

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.