ArticleMolecular and cellular biochemistry2016
A20 reduces lipid storage and inflammation in hypertrophic adipocytes via p38 and Akt signaling.
Article in Molecular and cellular biochemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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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.
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Who cites it
4 citing papers in PubMed, 8 citations in OpenAlex.
- Defective efferocytosis in diabetes: molecular mechanisms and emerging therapeutic strategies.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Review
- Protein posttranslational modifications in metabolic diseases: basic concepts and targeted therapies.MedComm · 2024Review
- Enhanced pathogenicity by up-regulation of A20 after avian leukemia subgroup a virus infection.Frontiers in veterinary science · 2022Article
- Effects of exosomes from LPS-activated macrophages on adipocyte gene expression, differentiation, and insulin-dependent glucose uptake.Journal of physiology and biochemistry · 2018Article
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Adipose tissue plays a vital role in the development of obesity and related disorders. Our previous study showed that A20, an ubiquitin-editing enzyme with anti-inflammation function, attenuated free fatty acids (FFAs)-induced lipid accumulation in nonalcoholic steatohepatitis. Here, we investigated A20 expression in adipose tissue of obese individuals and its effects on 3T3-L1 lipogenesis as well as the likely mechanisms underlying this process. By re-annotation of raw microarray data downloaded from Gene Expression Omnibus, we found that obese individuals showed significantly higher A20 mRNA levels in adipocytes. In vitro, A20 inhibited MCP-1 and IL-6 secretion in adipocytes. Forced expression of A20 resulted in decreased expression of key markers of lipogenesis and adipogenesis, such as sterol regulatory element binding protein 1c (SREBP-1c) and adipogenesis (aP2), leading to less lipids accumulation in differentiated 3T3-L1 cells. This process was concomitant with attenuated activation of p38 and Akt signaling. Our results suggest that A20 may have therapeutic potential for obesity and related diseases. The mechanisms involved the suppression of lipid storage and inflammation in adipocytes.
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Registered trials
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