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PINK1 Deficiency Facilitates Palmitic Acid-Induced Inflammation by Disrupting Mitochondrial Function to Activate
Bin Ye1,2, Yingting Pei1,2, Henian Li1,2
1Department of Biochemistry and Molecular Biology, Harbin Medical University, Harbin, China.
Abstract:
Metabolic cells exhibit low-grade chronic inflsammation characterized by excessive production and secretion of proinflammatory cytokines and chemokines in response to overnutrition and energy excess. Mitochondrial dysfunction is closely associated with metabolic inflammation. PINK1 (phosphatase and tensin homology-induced putative kinase 1) is a crucial pathway controlling mitochondrial autophagy, essential for maintaining mitochondrial quality control and metabolic homeostasis. The aim of this study was to investigate the role of PINK1 in metabolic inflammation. Our findings indicate that in adipocytes, palmitic acid (PA) activates the expression of PINK1. Additionally, knockdown of PINK1 exacerbates PA-induced adipocyte inflammation. Mechanistically, PINK1 deficiency impairs mitochondrial function, leading to the release of mtDNA and further activation of the cGAS-STING pathway. Therefore, targeting mitochondrial autophagy in adipocytes and the cGAS-STING pathway may represent effective approaches to alleviate the chronic inflammation associated with obesity and related metabolic disorders.
Insights
The study reveals that PINK1 (phosphatase and tensin homology-induced putative kinase 1) protects against palmitic acid-induced inflammation in adipocytes by maintaining mitochondrial health. Its deficiency worsens inflammation via the cGAS-STING pathway.
Area of Science:
- Cell Biology
- Metabolism
- Immunology
Background:
- Metabolic cells undergo chronic inflammation due to overnutrition, linked to mitochondrial dysfunction.
- PINK1 (phosphatase and tensin homology-induced putative kinase 1) is vital for mitochondrial autophagy and quality control, maintaining metabolic homeostasis.
Purpose of the Study:
- To investigate the role of PINK1 in metabolic inflammation within adipocytes.
Main Methods:
- Examined PINK1 expression in adipocytes exposed to palmitic acid (PA).
- Utilized PINK1 knockdown to assess its impact on PA-induced inflammation.
- Investigated mitochondrial function, mtDNA release, and the cGAS-STING pathway in PINK1-deficient adipocytes.
Main Results:
- Palmitic acid (PA) treatment increased PINK1 expression in adipocytes.
- Knockdown of PINK1 aggravated PA-induced adipocyte inflammation.
- PINK1 deficiency impaired mitochondrial function, increased mtDNA release, and activated the cGAS-STING pathway.
Conclusions:
- PINK1 plays a protective role against metabolic inflammation in adipocytes.
- Targeting mitochondrial autophagy and the cGAS-STING pathway could treat obesity-related chronic inflammation.
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