Evidence map›Paper›PMID 38245529›Full record

ArticleNature communications2024

Leukemia inhibitory factor suppresses hepatic de novo lipogenesis and induces cachexia in mice.

Xue Yang, Jianming Wang, Chun-Yuan Chang, Fan Zhou, Juan Liu, Huiting Xu, Maria Ibrahim, Maria Gomez, Grace L Guo, Hao Liu and 6 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
5.8field-weighted citation impact, top 3% 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

20 citing papers in PubMed, 1 synthesis or guideline pooled it, 25 citations in OpenAlex.

  1. Pooled it
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  11. Physical Activity, Exerkines, and Their Role in Cancer Cachexia.International journal of molecular sciences · 2025
    Review
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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

16 authors at 1 institution in 1 country.

Xue YangDepartment of Radiation Oncology, Rutgers Cancer Institute of New Jersey, Rutgers University, New Brunswick, NJ, USA.
Jianming WangDepartment of Radiation Oncology, Rutgers Cancer Institute of New Jersey, Rutgers University, New Brunswick, NJ, USA.ORCID 0000-0002-7265-1764
Chun-Yuan ChangDepartment of Radiation Oncology, Rutgers Cancer Institute of New Jersey, Rutgers University, New Brunswick, NJ, USA.ORCID 0000-0002-4562-9393
Fan ZhouDepartment of Radiation Oncology, Rutgers Cancer Institute of New Jersey, Rutgers University, New Brunswick, NJ, USA.
Juan LiuDepartment of Radiation Oncology, Rutgers Cancer Institute of New Jersey, Rutgers University, New Brunswick, NJ, USA.
Huiting XuDepartment of Medicine, Rutgers-Robert Wood Johnson Medical School, New Brunswick, NJ, USA.
Maria IbrahimRutgers Cancer Institute of New Jersey, Rutgers University, New Brunswick, NJ, USA.
Maria GomezRutgers Cancer Institute of New Jersey, Rutgers University, New Brunswick, NJ, USA.
Grace L GuoDepartment of Pharmacology and Toxicology, Rutgers University, Piscataway, NJ, USA.
Hao LiuDepartment of Biostatistics and Epidemiology, Rutgers School of Public Health, Piscataway, NJ, USA.
Wei-Xing ZongRutgers Cancer Institute of New Jersey, Rutgers University, New Brunswick, NJ, USA.
Fredric E WondisfordDepartment of Medicine, Rutgers-Robert Wood Johnson Medical School, New Brunswick, NJ, USA.
Xiaoyang SuDepartment of Medicine, Rutgers-Robert Wood Johnson Medical School, New Brunswick, NJ, USA.ORCID 0000-0001-8081-1396
Eileen WhiteRutgers Cancer Institute of New Jersey, Rutgers University, New Brunswick, NJ, USA.ORCID 0000-0003-2961-3065
Zhaohui FengDepartment of Radiation Oncology, Rutgers Cancer Institute of New Jersey, Rutgers University, New Brunswick, NJ, USA. fengzh@cinj.rutgers.edu.ORCID 0000-0002-8912-6456
Wenwei HuDepartment of Radiation Oncology, Rutgers Cancer Institute of New Jersey, Rutgers University, New Brunswick, NJ, USA. wh221@cinj.rutgers.edu.ORCID 0000-0003-3971-4257
Rutgers, The State University of New Jersey · US

Funding

Translational Research Support CoreP30ES005022 · NIEHS · UNIV OF MED/DENT NJ-R W JOHNSON MED SCH · PI HELMUT ZARBL · 1988 to 2026
$47.4M
Glutamine synthetase in cancer cell metabolism and oncogenesisR01CA224550 · NCI · RUTGERS, THE STATE UNIV OF N.J. · PI Wei-Xing Zong · 2018 to 2026
$4.7M
CANCAN-RUTGERSOT2CA278609 · NCI · RUTGERS BIOMEDICAL AND HEALTH SCIENCES · PI Eileen P. White · 2022 to 2026
$2.6M
Gain-of-function mutant p53 and metabolic reprogramming in colorectal cancerR01CA260837 · NCI · RUTGERS BIOMEDICAL AND HEALTH SCIENCES · PI FENG, ZHAOHUI, HU, WENWEI · 2021 to 2025
$2.2M
The role of leukemia inhibitory factor in colorectal cancerR01CA260838 · NCI · RUTGERS BIOMEDICAL AND HEALTH SCIENCES · PI Wenwei Hu · 2022 to 2026
$1.9M
SENP6, a novel p53 negative regulator, is an important new player in cancerR01CA214746 · NCI · RUTGERS BIOMEDICAL AND HEALTH SCIENCES · PI FENG, ZHAOHUI · 2018 to 2022
$1.8M
Metabolic reprogramming in breast cancerR01CA227912 · NCI · RBHS -CANCER INSTITUTE OF NEW JERSEY · PI FENG, ZHAOHUI, HU, WENWEI · 2018 to 2022
$1.8M
Gut-liver crosstalk by FGF15/19 in regulating xenobiotic nuclear receptor activationR01GM135258 · NIGMS · RUTGERS, THE STATE UNIV OF N.J. · PI GUO, GRACE L · 2020 to 2023
$1.4M
Role of Intestinal Bile Acid Signaling in Liver DiseasesI01BX002741 · VA · VA NEW JERSEY HEALTH CARE SYSTEM · PI GRACE L GUO · 2018 to 2026
–
BLRD VA I01 BX002741Cancer Research UK CGCATF-2021/100026NCI NIH HHS OT2 CA278609NCI NIH HHS R01 CA214746NCI NIH HHS R01 CA224550NCI NIH HHS R01 CA227912NCI NIH HHS R01 CA260837NCI NIH HHS R01 CA260838NIEHS NIH HHS P30 ES005022NIGMS NIH HHS R01 GM135258
6 · The paper itself

Abstract

Cancer cachexia is a systemic metabolic syndrome characterized by involuntary weight loss, and muscle and adipose tissue wasting. Mechanisms underlying cachexia remain poorly understood. Leukemia inhibitory factor (LIF), a multi-functional cytokine, has been suggested as a cachexia-inducing factor. In a transgenic mouse model with conditional LIF expression, systemic elevation of LIF induces cachexia. LIF overexpression decreases de novo lipogenesis and disrupts lipid homeostasis in the liver. Liver-specific LIF receptor knockout attenuates LIF-induced cachexia, suggesting that LIF-induced functional changes in the liver contribute to cachexia. Mechanistically, LIF overexpression activates STAT3 to downregulate PPARα, a master regulator of lipid metabolism, leading to the downregulation of a group of PPARα target genes involved in lipogenesis and decreased lipogenesis in the liver. Activating PPARα by fenofibrate, a PPARα agonist, restores lipid homeostasis in the liver and inhibits LIF-induced cachexia. These results provide valuable insights into cachexia, which may help develop strategies to treat cancer cachexia.

Indexed as

CachexiaNeoplasmsAnimalsLeukemia Inhibitory FactorLipidsLipogenesisLiverMiceMice, TransgenicPPAR alphaLeukemia Inhibitory FactorLif protein, mouseLipidsPPAR alpha

Identifiers

PMID38245529
PMCPMC10799847
OpenAlexW4391051427

What OpenQuestion holds

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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.