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Updated: Sep 11, 2025

A Human Ex Vivo Atherosclerotic Plaque Model to Study Lesion Biology
Published on: May 6, 2014
JNK in inflammation and lipid metabolism regulation in atherosclerosis
Dan Tang1, Yi Yao2, Xing Xiang1
1Department of Clinical Laboratory Medicine, Institution of microbiology and infectious diseases, The First Affiliated Hospital, Hengyang Medical School, University of South China, Hengyang, Hunan, China; Hunan Provincial Key Laboratory of Multi-omics And Artificial Intelligence of Cardiovascular Diseases, University of South China, Hengyang, Hunan, China; Clinical Research Center for Myocardial Injury in Hunan Province, Hengyang, Hunan, China; Institute of Cardiovascular Disease, The First Affiliated Hospital, Hengyang Medical School, University of South China, Hengyang, Hunan, China.
Abstract:
Atherosclerosis is a systemic arterial disease characterized by lipid deposition, chronic inflammation, and endothelial dysfunction and is driven by complex, multifactorial regulation. c-Jun N-terminal kinase (JNK), a key member of the stress-activated mitogen-activated protein kinase family, plays a central role in pathogenesis. JNK regulates oxidative stress, lipid metabolism, and inflammation by mediating interactions between cells and organs. For example, vascular injury activates JNK, triggering downstream pathways that amplify inflammation and accelerate disease progression. JNK also indirectly influences vascular health by modulating metabolic and inflammatory processes in organs such as the liver and kidneys, underscoring interorgan synergy. This review highlights the potential of JNK as a therapeutic target for atherosclerosis. Understanding this pathway may help develop effective treatments for this complex systemic disease.
Insights
Atherosclerosis involves complex regulation, with c-Jun N-terminal kinase (JNK) central to its development. Targeting JNK may offer new treatments for this systemic arterial disease.
Area of Science:
- Cardiovascular Biology
- Molecular Medicine
- Pathophysiology
Background:
- Atherosclerosis is a systemic arterial disease marked by lipid buildup, inflammation, and endothelial dysfunction.
- Complex, multifactorial regulation drives atherosclerosis pathogenesis.
- c-Jun N-terminal kinase (JNK), a stress-activated kinase, is implicated in disease development.
Purpose of the Study:
- To review the role of JNK in atherosclerosis.
- To highlight JNK as a potential therapeutic target for atherosclerosis.
Main Methods:
- This is a review article, synthesizing existing research on JNK's role in atherosclerosis.
- Literature review focusing on molecular mechanisms and interorgan effects.
Main Results:
- JNK regulates key pathogenic processes including oxidative stress, lipid metabolism, and inflammation.
- Vascular injury activates JNK, amplifying inflammation and disease progression.
- JNK influences vascular health via metabolic and inflammatory pathways in organs like the liver and kidneys.
Conclusions:
- JNK plays a central role in the pathogenesis of atherosclerosis.
- Targeting JNK pathways presents a promising therapeutic strategy for atherosclerosis.
- Understanding JNK's interorgan effects is crucial for developing effective treatments.
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