Evidence map›Paper›PMID 40038775›Full record

ArticleMilitary Medical Research2025

Motor protein KIF13B orchestrates hepatic metabolism to prevent metabolic dysfunction-associated fatty liver disease.

Guo-Lin Miao, Wen-Xi Zhang, Yi-Tong Xu, Yi-Ran Liu, Ping-Ping Lai, Jia-Bao Guo, Gong-Lie Chen, Jing-Xuan Chen, Zi-Hao Zhou, Yan-Wei Li and 16 more

Abstract read
In one paragraph

Article in Military Medical Research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing 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

10 citing papers in PubMed.

  1. Article
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  3. 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

26 authors.

Guo-Lin Miao *Institute of Cardiovascular Sciences, State Key Laboratory of Vascular Homeostasis and Remodeling, School of Basic Medical Sciences, Peking University, Beijing, 100191, China.
Wen-Xi Zhang *Institute of Cardiovascular Sciences, State Key Laboratory of Vascular Homeostasis and Remodeling, School of Basic Medical Sciences, Peking University, Beijing, 100191, China.
Yi-Tong Xu *Institute of Cardiovascular Sciences, State Key Laboratory of Vascular Homeostasis and Remodeling, School of Basic Medical Sciences, Peking University, Beijing, 100191, China.
Yi-Ran Liu *Department of Biomedical Informatics, State Key Laboratory of Vascular Homeostasis and Remodeling, School of Basic Medical Sciences, Peking University, Beijing, 100191, China.
Ping-Ping LaiInstitute of Cardiovascular Sciences, State Key Laboratory of Vascular Homeostasis and Remodeling, School of Basic Medical Sciences, Peking University, Beijing, 100191, China.
Jia-Bao GuoInstitute of Cardiovascular Sciences, State Key Laboratory of Vascular Homeostasis and Remodeling, School of Basic Medical Sciences, Peking University, Beijing, 100191, China.
Gong-Lie ChenInstitute of Cardiovascular Sciences, State Key Laboratory of Vascular Homeostasis and Remodeling, School of Basic Medical Sciences, Peking University, Beijing, 100191, China.
Jing-Xuan ChenInstitute of Cardiovascular Sciences, State Key Laboratory of Vascular Homeostasis and Remodeling, School of Basic Medical Sciences, Peking University, Beijing, 100191, China.
Zi-Hao ZhouInstitute of Cardiovascular Sciences, State Key Laboratory of Vascular Homeostasis and Remodeling, School of Basic Medical Sciences, Peking University, Beijing, 100191, China.
Yan-Wei LiDepartment of Infectious Diseases, Shengjing Hospital of China Medical University, Shenyang, 110134, China.
Chong ZhangDepartment of Infectious Diseases, Shengjing Hospital of China Medical University, Shenyang, 110134, China.
Yang DingDepartment of Infectious Diseases, Shengjing Hospital of China Medical University, Shenyang, 110134, China.
Lian-Xin ZhangInstitute of Cardiovascular Sciences, State Key Laboratory of Vascular Homeostasis and Remodeling, School of Basic Medical Sciences, Peking University, Beijing, 100191, China.
Yu-Fei HanInstitute of Cardiovascular Sciences, State Key Laboratory of Vascular Homeostasis and Remodeling, School of Basic Medical Sciences, Peking University, Beijing, 100191, China.
Jin-Xuan ChenInstitute of Cardiovascular Sciences, State Key Laboratory of Vascular Homeostasis and Remodeling, School of Basic Medical Sciences, Peking University, Beijing, 100191, China.
Jing-Dong WuState Key Laboratory of Natural and Biomimetic Drugs, Ministry of Education, Key Laboratory of Cell Proliferation and Differentiation, Beijing Key Laboratory of Cardiometabolic Molecular Medicine, Center for Life Sciences, Institute of Molecular Medicine, College of Future Technology, Peking University, Beijing, 100871, China.
Yin-Qi ZhaoInstitute of Cardiovascular Sciences, State Key Laboratory of Vascular Homeostasis and Remodeling, School of Basic Medical Sciences, Peking University, Beijing, 100191, China.
Si MeiInstitute of Cardiovascular Sciences, State Key Laboratory of Vascular Homeostasis and Remodeling, School of Basic Medical Sciences, Peking University, Beijing, 100191, China.
Yang ZhaoState Key Laboratory of Natural and Biomimetic Drugs, Ministry of Education, Key Laboratory of Cell Proliferation and Differentiation, Beijing Key Laboratory of Cardiometabolic Molecular Medicine, Center for Life Sciences, Institute of Molecular Medicine, College of Future Technology, Peking University, Beijing, 100871, China.
Yuan-Wu MaKey Laboratory of Human Disease Comparative Medicine, National Health Commission of China (NHC), Beijing Engineering Research Center for Experimental Animal Models of Human Critical Diseases, Institute of Laboratory Animal Science, Chinese Academy of Medical Sciences, Peking Union Medicine College, Beijing, 100021, China.
Ling ZhangInstitute of Cardiovascular Sciences, State Key Laboratory of Vascular Homeostasis and Remodeling, School of Basic Medical Sciences, Peking University, Beijing, 100191, China.
Wei HuangInstitute of Cardiovascular Sciences, State Key Laboratory of Vascular Homeostasis and Remodeling, School of Basic Medical Sciences, Peking University, Beijing, 100191, China.
Dong-Yu ZhaoDepartment of Biomedical Informatics, State Key Laboratory of Vascular Homeostasis and Remodeling, School of Basic Medical Sciences, Peking University, Beijing, 100191, China. zhaodongyu@bjmu.edu.cn.
Er-Dan DongInstitute of Cardiovascular Sciences, State Key Laboratory of Vascular Homeostasis and Remodeling, School of Basic Medical Sciences, Peking University, Beijing, 100191, China. donged@bjmu.edu.cn.
Yu-Hui WangInstitute of Cardiovascular Sciences, State Key Laboratory of Vascular Homeostasis and Remodeling, School of Basic Medical Sciences, Peking University, Beijing, 100191, China. wangyuhui2009@bjmu.edu.cn.
Xun-De XianInstitute of Cardiovascular Sciences, State Key Laboratory of Vascular Homeostasis and Remodeling, School of Basic Medical Sciences, Peking University, Beijing, 100191, China. xianxunde@bjmu.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundKinesin family member 13B (KIF13B), a crucial motor protein, exerts multiple cellular biological functions. However, the implication of KIF13B in metabolic dysfunction-associated fatty liver disease (MAFLD) has not been explored yet. This study aimed to investigate KIF13B's role and underlying mechanism in MAFLD and proposes it as a potential pharmacological target.

methodsWe assessed KIF13B expression in MAFLD patients and rodent models. The roles of Kif13b in lipid metabolism and MAFLD were investigated using whole-body Kif13b knockout mice, hepatocyte-specific Kif13b-deficient mice and hamsters exposed to different diets. The underlying mechanisms by which Kif13b governed hepatic lipid homeostasis and MAFLD progression were explored in vitro. Finally, the Kif13b's impact on atherosclerotic development was studied in the context of MAFLD.

resultsKIF13B expression was reduced in patients and murine models with MAFLD. Rodents with global or liver-specific knockout of the Kif13b gene exhibit spontaneous hepatic steatosis, which is further exacerbated by different overnutrition diets. Overexpression of human KIF13B by lentivirus effectively prevented metabolic dysfunction-associated steatohepatitis (MASH) in methionine-choline-deficient diet (MCD)-fed mice. Furthermore, Kif13b deficiency accelerates atherosclerosis in the context of MAFLD. Mechanistically, Kif13b depletion increases hepatic lipid synthesis and impairs mitochondrial oxidative phosphorylation. Further screening reveals that Kif13b interacts with AMP-activated catalytic subunit alpha 1 (AMPKα1) to regulate the phosphorylation of AMPKα1, governing mitochondrial homeostasis and suppressing sterol regulatory element binding protein 1 (Srebp1)-mediated de novo lipogenesis in the liver.

conclusionThis work establishes a causal relationship between KIF13B deficiency and MAFLD, emphasizing KIF13B as a potential therapeutic target for treating MAFLD.

Indexed as

Fatty LiverKinesinsLiverAnimalsCricetinaeDisease Models, AnimalHumansLipid MetabolismMaleMiceMice, Inbred C57BLMice, KnockoutKinesinsAMP-activated catalytic subunit alpha 1Kinesin family member 13BLipid metabolismMetabolic dysfunction-associated fatty liver diseaseMitochondrial homeostasis

Identifiers

PMID40038775
PMCPMC11877712

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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.