Academic Journal
The central role of mitochondrial metabolism in hepatic steatosis
| العنوان: | The central role of mitochondrial metabolism in hepatic steatosis |
|---|---|
| المؤلفون: | Sanda Win, Tin Aung Than, Neil Kaplowitz, Nicole Wong, Aliza Arya, Zin Thandar Win, Shwe Hlaing Win, Ei Hnin Phyu, Christina Kuemerle, Jake Suh, Sona Avanesyan, Pujan Prakash Dobaria, Hnin Wai Lwin, Sean Wong, Shannon Kaw, Samuel Wong, Kyaw Khaing Soe, Garmani Kyaw, Filbert Win Min Aung |
| المصدر: | Exploration of Digestive Diseases, Vol 3, Iss 1, Pp 42-68 (2024) |
| بيانات النشر: | Open Exploration Publishing Inc. |
| سنة النشر: | 2024 |
| المجموعة: | Directory of Open Access Journals: DOAJ Articles |
| مصطلحات موضوعية: | tricarboxylic acid cycle (tca cycle), citric acid, acetyl-coa, sh3 domain-binding protein 5 (sab/sh3bp5), c-jun n-terminal kinase (jnk), metabolic adaptation, lipogenesis, Diseases of the digestive system. Gastroenterology, RC799-869 |
| الوصف: | Mitochondria are present in all mammalian cells except matured red blood cells. Mitochondria consist of several metabolic pathways for glucose, fatty acids, amino acids, and bioenergetic pathways for ATP synthesis, membrane potential, and reactive oxygen production. In the liver, hepatic mitochondria play a key role in hepatic steatosis because mitochondrial metabolism produces acetyl-CoA which is the building block for synthesis of lipids and cholesterol. Mitochondria inner membrane is impermeable of metabolites, reducing equivalents, and small molecules such as phosphate, and sulfate. Thus, mitochondrial shuttles and carriers function as the routes of influx and efflux of these metabolites and molecules across the inner membrane. The signal regulation of these shuttles and mitochondrial enzymes could play a key role in coordinating the mitochondrial metabolism to adapt the cytosolic part of metabolic pathways in liver metabolic stress. Intriguingly, the interaction of mitochondria protein SH3 domain-binding protein 5 (SAB/SH3BP5) and c-Jun N-terminal kinase (JNK) was found as a pivotal role in sustained activation of JNK and phosphorylated-JNK (P-JNK) mediated activation of lipogenic pathway in nutritional excess. Knockout or knockdown of SAB prevented or reversed the hepatic steatosis, inflammation, and fibrosis, and improved metabolic intolerance and energy expenditure. Moreover, blocking the SAB peptide prevents palmitic acid-induced P-JNK interaction with SAB and inhibition of mitochondrial bioenergetics, implying the P-JNK effect on mitochondrial metabolism. This review focuses on the flow of mitochondrial metabolites in metabolic stress conditions and the contribution of mitochondria and mitochondrial stress signals in hepatic steatosis. |
| نوع الوثيقة: | article in journal/newspaper |
| اللغة: | English |
| تدمد: | 2833-6321 |
| Relation: | https://www.explorationpub.com/Journals/edd/Article/100539; https://doaj.org/toc/2833-6321; https://doaj.org/article/1ebf96b0fd424014ae0a8d147fd50ef5 |
| DOI: | 10.37349/edd.2024.00039 |
| الاتاحة: | https://doi.org/10.37349/edd.2024.00039 https://doaj.org/article/1ebf96b0fd424014ae0a8d147fd50ef5 |
| رقم الانضمام: | edsbas.AE89E569 |
| قاعدة البيانات: | BASE |
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