ArticleInternational journal of molecular sciences2022
Loss of TRIM67 Attenuates the Progress of Obesity-Induced Non-Alcoholic Fatty Liver Disease.
Article in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 20 citations in OpenAlex.
- Roles and Mechanisms of TRIM Family Proteins in Inflammation in the Brain and Beyond.International journal of molecular sciences · 2026Review
- The Impact ofMicroorganisms · 2025Article
- The emerging role of E3 ubiquitin ligases and deubiquitinases in metabolic dysfunction-associated steatotic liver disease.Journal of translational medicine · 2025Review
- The ubiquitin-proteasome system: A potential target for the MASLD.Acta pharmaceutica Sinica. B · 2025Review
- Extracellular vesicle transfer of miR-1 to adipose tissue modifies lipolytic pathways following resistance exercise.JCI insight · 2024Article
- TRIM Proteins and Antiviral Microtubule Reorganization: A Novel Component in Innate Immune Responses?Viruses · 2024Review
- PGC-1α-Coordinated Hypothalamic Antioxidant Defense Is Linked to SP1-LanCL1 Axis during High-Fat-Diet-Induced Obesity in Male Mice.Antioxidants (Basel, Switzerland) · 2024Article
- Article
- TRIM67 Implicates in Regulating the Homeostasis and Synaptic Development of Mitral Cells in the Olfactory Bulb.International journal of molecular sciences · 2023Article
- Article
- The role of TRIM family in metabolic associated fatty liver disease.Frontiers in endocrinology · 2023Review
- Review
- Polysaccharide fromInternational journal of molecular sciences · 2022Article
- The Related Metabolic Diseases and Treatments of Obesity.Healthcare (Basel, Switzerland) · 2022Review
- TRIM67 Deficiency Exacerbates Hypothalamic Inflammation and Fat Accumulation in Obese Mice.International journal of molecular sciences · 2022Article
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Authors and funding
14 authors at 1 institution in 1 country.
Funding
Abstract
Obesity is considered as a major cause for the development and progress of non-alcoholic fatty liver disease (NAFLD), which is one of the most prevalent chronic liver diseases worldwide. However, molecular mechanisms that implicate in obesity-driven pathophysiology of NAFLD are not well defined. Here, we report a tripartite motif (TRIM) protein family member-TRIM67-that is hardly expressed in liver but is inducible on obese conditions. Enhanced expression of TRIM67 activates hepatic inflammation to disturb lipid metabolic homeostasis and promote the progress of NAFLD induced by obesity, while the deficiency in TRIM67 is protective against these pathophysiological processes. Finally, we show that the important transcription coactivator PGC-1α implicates in the response of hepatic TRIM67 to obesity.
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