Evidence map›Paper›PMID 41638479›Full record

ArticleCellular and molecular gastroenterology and hepatology2026

Overlapping Yet Distinct Functions of Vacuole Membrane Protein 1 and Transmembrane Protein 41B in Modulating Hepatic Lipoprotein Secretion and Autophagy.

Allen Chen, Khue Nguyen, Mengwei Niu, Xiaoxiao Jiang, Xiaochen Yu, Yan Xie, Wanqing Liu, Nicholas O Davidson, Wen-Xing Ding, Hong-Min Ni

Abstract read
In one paragraph

Article in Cellular and molecular gastroenterology and hepatology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
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

2 citing papers in PubMed.

  1. Article
  2. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors.

Allen ChenDepartment of Pharmacology, Toxicology and Therapeutics, University of Kansas Medical Center, Kansas City, Kansas.
Khue NguyenDepartment of Pharmacology, Toxicology and Therapeutics, University of Kansas Medical Center, Kansas City, Kansas.
Mengwei NiuDepartment of Pharmacology, Toxicology and Therapeutics, University of Kansas Medical Center, Kansas City, Kansas.
Xiaoxiao JiangDepartment of Pharmacology, Toxicology and Therapeutics, University of Kansas Medical Center, Kansas City, Kansas.
Xiaochen YuDepartment of Pharmacology, Toxicology and Therapeutics, University of Kansas Medical Center, Kansas City, Kansas.
Yan XieDivision of Gastroenterology, Department of Medicine, Washington University School of Medicine, St Louis, Missouri.
Wanqing LiuDepartment of Pharmaceutical Sciences, Wayne State University, Detroit, Michigan.
Nicholas O DavidsonDivision of Gastroenterology, Department of Medicine, Washington University School of Medicine, St Louis, Missouri.
Wen-Xing DingDepartment of Pharmacology, Toxicology and Therapeutics, University of Kansas Medical Center, Kansas City, Kansas; Department of Internal Medicine, University of Kansas Medical Center, Kansas City, Kansas.
Hong-Min NiDepartment of Pharmacology, Toxicology and Therapeutics, University of Kansas Medical Center, Kansas City, Kansas. Electronic address: hni@kumc.edu.

Funding

Triglycerides, Diabetes and Cardiovascular DiseaseP01HL151328 · NHLBI · UNIVERSITY OF WASHINGTON · PI Karin E Bornfeldt · 2020 to 2026
$19.6M
Impaired VLDL secretion, progression and reversal of hepatic fibrogenesisR01DK119437 · NIDDK · WASHINGTON UNIVERSITY · PI Nicholas O. Davidson · 2019 to 2026
$3.8M
Mechanisms regulating autophagy in alcohol-induced liver injuryR37AA020518 · NIAAA · UNIVERSITY OF KANSAS MEDICAL CENTER · PI Wen-Xing Ding · 2019 to 2026
$3.2M
Interaction between Genome and Heavy Metals in Nonalcoholic Fatty Liver DiseaseR01ES034410 · NIEHS · WAYNE STATE UNIVERSITY · PI Andrea E Cassidy-Bushrow, Wanqing Liu · 2023 to 2026
$2.4M
A Precision Targeted Therapeutics for Nonalcoholic Fatty Liver DiseaseR01DK124612 · NIDDK · WAYNE STATE UNIVERSITY · PI LIU, WANQING · 2021 to 2024
$1.7M
Mechanisms of mitochondrial dynamics, quality control and mtDNA-mediated inflammation in alcohol-associated liver diseaseR01AA031230 · NIAAA · UNIVERSITY OF KANSAS MEDICAL CENTER · PI Wen-Xing Ding · 2024 to 2026
$1.2M
Translating Obesity, Metabolic Dysfunction and Comorbid Disease StatesT32DK128770 · NIDDK · UNIVERSITY OF KANSAS MEDICAL CENTER · PI John P Thyfault, Douglas E Wright · 2022 to 2026
$806k
Novel mechanisms regulating VLDL secretion and non-alcoholic fatty liver diseasesR56DK129234 · NIDDK · UNIVERSITY OF KANSAS MEDICAL CENTER · PI NI, HONGMIN · 2021 to 2021
$402k
NHLBI NIH HHS P01 HL151328NIAAA NIH HHS R01 AA031230NIAAA NIH HHS R37 AA020518NIDDK NIH HHS R01 DK119437NIDDK NIH HHS R01 DK124612NIDDK NIH HHS R56 DK129234NIDDK NIH HHS T32 DK128770NIEHS NIH HHS R01 ES034410
6 · The paper itself

Abstract

BACKGROUND &

aimsTransmembrane protein 41B (TMEM41B) and vacuolar membrane protein 1 (VMP1) are endoplasmic reticulum (ER) scramblases whose roles in hepatic lipoprotein secretion and autophagy in metabolic-associated steatotic liver disease (MASLD) remain unclear.

methodsWe undertook lipidomic and functional studies in liver- and hepatocyte-specific Tmem41b knockout (KO) mice; Tmem41b knock-in (KI) mice, Tmem41b/Vmp1 double KO (DKO); Tmem41b KO/Vmp1 KI, and Vmp1 KO/Tmem41b KI mice.

resultsTMEM41B protein levels decreased in the livers of human subjects with MASLD. Loss of hepatic Tmem41b impaired very low-density lipoprotein (VLDL) secretion, with steatosis, inflammation, and fibrosis, whereas hepatic TMEM41B overexpression mitigated these effects. Tmem41b/Vmp1 DKO mice showed further impairment in VLDL secretion compared with single Tmem41b KO. Lipidomic analysis revealed decreased phosphatidylcholine and phosphatidylethanolamine, with increased neutral lipids in Tmem41b KO mice. VMP1 and TMEM41B localize at the mitochondrial-associated membrane with reduced mitochondria-ER contact in Vmp1 and Tmem41b KO mice. Loss of hepatic VMP1 or TMEM41B increased levels of LC3B-II and p62/SQSTM1, which were not further changed in DKO mice. Restoring VMP1 in Tmem41b KO mice and TMEM41B in Vmp1 KO mice partially corrected defective VLDL secretion and hepatic steatosis in these single KO mice, respectively. Restoring VMP1 at a low but not a high dose corrected defective autophagy in Tmem41b KO mice, whereas overexpression of TMEM41B dose-dependently improved defective autophagy in Vmp1 KO mice.

conclusionsLoss of hepatic VMP1 or TMEM41B reduces VLDL secretion and promotes MASLD via overlapping but distinct mechanisms that regulate lipoprotein secretion and autophagy.

Indexed as

AutophagyFatty LiverLipoproteins, VLDLLiverMembrane ProteinsPhospholipid Transfer ProteinsAnimalsDisease Models, AnimalEndoplasmic ReticulumHepatocytesHumansMaleMiceMice, KnockoutLipoproteins, VLDLMembrane ProteinsPhospholipid Transfer ProteinsTMEM41B protein, humanVMP1 protein, humanEndoplasmic ReticulumLiver InjuryMASLDSteatosisVLDL Secretion

Identifiers

PMID41638479
PMCPMC13090722

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Registered trials

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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.