Evidence map›Paper›PMID 40846699›Full record

ArticleCell death discovery2025

Cold-induced hepatocyte-derived exosomes activate brown adipose thermogenesis via miR-293-5p-mediated transcriptional reprogramming.

Xiujuan Gao, Junqing Xu, Zengqiang Xu, Mengxin Jiang, Jiahao Zhu, Yang Geng, Shengjun Dong, Yanuo Li, Zhengtong Zhou, Yingjiang Xu

Abstract read
In one paragraph

Article in Cell death discovery, 2025. 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

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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. Review
  2. Review
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

10 authors.

Xiujuan Gao *Binzhou Medical University Hospital, Binzhou City, PR China.
Junqing Xu *Binzhou Medical University Hospital, Binzhou City, PR China.
Zengqiang Xu *Binzhou Medical University Hospital, Binzhou City, PR China.
Mengxin JiangBinzhou Medical University Hospital, Binzhou City, PR China.
Jiahao ZhuBinzhou Medical University Hospital, Binzhou City, PR China.
Yang GengBinzhou Medical University Hospital, Binzhou City, PR China.
Shengjun DongBinzhou Medical University Hospital, Binzhou City, PR China.
Yanuo LiDepartment of Pathophysiology, School of Basic Medicine, Binzhou Medical University, Yantai City, PR China. liyanuo@bzmc.edu.cn.
Zhengtong ZhouInstitute of Medical Genomics, Biomedical Sciences College & Shandong Medicinal Biotechnology Centre, Medical Science and Technology Innovation Center, Shandong First Medical University & Shandong Academy of Medical Sciences, Jinan City, PR China. drzhoujiaqing@126.com.
Yingjiang XuBinzhou Medical University Hospital, Binzhou City, PR China. xuyingjiang1214@126.com.ORCID http://orcid.org/0000-0001-6492-9132

Funding

Natural Science Foundation of Shandong Province (Shandong Provincial Natural Science Foundation) ZR2022QH358
6 · The paper itself

Abstract

The liver-adipose axis represents a crucial regulatory network that governs systemic lipid homeostasis, with signals originating from the liver orchestrating the plasticity of adipose tissue through diverse mechanisms. A comprehensive understanding of these bidirectional communication pathways may uncover novel therapeutic approaches for metabolic disorders. Our research demonstrates that exposure to cold stimulates the liver to secrete exosomes, which enhance thermogenic activation in adipose tissue, as observed in both in vitro and in vivo models. This enhancement of thermogenesis is mechanistically associated with the cold-induced upregulation of hepatocyte-derived exosomal miR-293-5p. Importantly, the pharmacological administration of a miR-293-5p agomir significantly mitigates diet-induced obesity and related metabolic dysfunctions in murine models. Through mechanistic analysis, we identified Tet1 as a direct downstream target of miR-293-5p, noting that the ectopic expression of Tet1 disrupts the thermogenic programming of brown adipose tissue (BAT) independently of miR-293-5p modulation. Our findings establish cold-activated hepatocyte exosomes as endocrine signaling mediators that carry thermogenic microRNA cargos, with miR-293-5p emerging as a key regulator.

Identifiers

PMID40846699
PMCPMC12373855

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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.