Evidence map›Paper›PMID 39009585›Full record

ArticleCell death discovery2024

FADD regulates adipose inflammation, adipogenesis, and adipocyte survival.

Jianlei Tang, Yue Ma, Meilin Li, Xiangpeng Liu, Yuting Wang, Jie Zhang, Hui Shu, Zhiwei Liu, Chi Zhang, Lei Fu and 4 more

Abstract read
In one paragraph

Article in Cell death discovery, 2024. 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. Review
  2. Article
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

14 authors.

Jianlei Tang *Department of Endocrinology, The Second Affiliated Hospital of Soochow University, Suzhou, China.
Yue Ma *Cambridge-Suda Genomic Resource Center, Suzhou Medical School, Soochow University, Suzhou, China.
Meilin Li *Cambridge-Suda Genomic Resource Center, Suzhou Medical School, Soochow University, Suzhou, China.
Xiangpeng LiuCambridge-Suda Genomic Resource Center, Suzhou Medical School, Soochow University, Suzhou, China.
Yuting WangDepartment of Endocrinology, The Second Affiliated Hospital of Soochow University, Suzhou, China.
Jie ZhangCambridge-Suda Genomic Resource Center, Suzhou Medical School, Soochow University, Suzhou, China.
Hui ShuCambridge-Suda Genomic Resource Center, Suzhou Medical School, Soochow University, Suzhou, China.
Zhiwei LiuCambridge-Suda Genomic Resource Center, Suzhou Medical School, Soochow University, Suzhou, China.
Chi ZhangCambridge-Suda Genomic Resource Center, Suzhou Medical School, Soochow University, Suzhou, China.
Lei FuWisdom Lake Academy of Pharmacy, Xi'an Jiaotong-Liverpool University, Suzhou, China.ORCID http://orcid.org/0000-0002-0802-6446
Ji HuDepartment of Endocrinology, The Second Affiliated Hospital of Soochow University, Suzhou, China. huji@suda.edu.cn.ORCID http://orcid.org/0000-0002-3443-999X
Yong ZhangCambridge-Suda Genomic Resource Center, Suzhou Medical School, Soochow University, Suzhou, China. yong.zhang@suda.edu.cn.ORCID http://orcid.org/0000-0002-0936-9264
Zhihao JiaCambridge-Suda Genomic Resource Center, Suzhou Medical School, Soochow University, Suzhou, China. zhjia@suda.edu.cn.ORCID http://orcid.org/0000-0001-5525-2721
Yu FengDepartment of Endocrinology, The Second Affiliated Hospital of Soochow University, Suzhou, China. fengyu1980@suda.edu.cn.ORCID http://orcid.org/0000-0003-0034-6397

Funding

National Natural Science Foundation of China (National Science Foundation of China) 82070838Natural Science Foundation of Jiangsu Province (Jiangsu Provincial Natural Science Foundation) BK20210a715
6 · The paper itself

Abstract

Adipose tissue, aside from adipocytes, comprises various abundant immune cells. The accumulation of low-grade chronic inflammation in adipose tissue serves as a primary cause and hallmark of insulin resistance. In this study, we investigate the physiological roles of FADD in adipose tissue inflammation, adipogenesis, and adipocyte survival. High levels of Fadd mRNA were observed in mitochondrial-rich organs, particularly brown adipose tissue. To explore its metabolic functions, we generated global Fadd knockout mice, resulting in embryonic lethality, while heterozygous knockout (Fadd+/-) mice did not show any significant changes in body weight or composition. However, Fadd+/- mice exhibited reduced respiratory exchange ratio (RER) and serum cholesterol levels, along with heightened global and adipose inflammatory responses. Furthermore, AT masses and expression levels of adipogenic and lipogenic genes were decreased in Fadd+/- mice. In cellular studies, Fadd inhibition disrupted adipogenic differentiation and suppressed the expression of adipogenic and lipogenic genes in cultured adipocytes. Additionally, Fadd overexpression caused adipocyte death in vitro with decreased RIPK1 and RIPK3 expression, while Fadd inhibition downregulated RIPK3 in iWAT in vivo. These findings collectively underscore the indispensable role of FADD in adipose inflammation, adipogenesis, and adipocyte survival.

Identifiers

PMID39009585
PMCPMC11250791

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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.