Krebs Cycle Rewired: Driver of Atherosclerosis Progression?

Yamin Liang; Yanmei Chen; Lu Li; Shulei Zhang; Jinyan Xiao; Dangheng Wei

doi:10.2174/0929867328666210806105246

Krebs Cycle Rewired: Driver of Atherosclerosis Progression?

Curr Med Chem. 2022;29(13):2322-2333. doi: 10.2174/0929867328666210806105246.

Authors

Yamin Liang¹, Yanmei Chen¹, Lu Li¹, Shulei Zhang¹, Jinyan Xiao², Dangheng Wei¹

Affiliations

¹ Institute of Cardiovascular Disease, Key Laboratory for Arteriosclerology of Hunan Province, Hunan International Scientific and Technological Cooperation Base of Arteriosclerotic Disease, Hengyang Medical College, University of South China, Hengyang, Hunan 421001, China.
² YueYang Maternal-Child Medicine Health Hospital Hunan, Province Innovative Training Base for Medical Postgraduates, University of China South China and Yueyang Women & Children's Medical Center, Yueyang, Hunan, 414000, China.

PMID: 34365937
DOI: 10.2174/0929867328666210806105246

Abstract

The tricarboxylic acid (TCA) cycle is the center of energy metabolism in eukaryotic cells and is dynamically adjusted according to the energy needs of cells. Macrophages are activated by inflammatory stimuli, and then two breakpoints in TCA cycle lead to the accumulation of intermediates. Atherosclerosis is a chronic inflammatory process. Here, the "non-metabolic" signaling functions of TCA cycle intermediates in the macrophage under inflammatory stimulation and the role of intermediates in the progression of atherosclerosis are discussed.

Keywords: GPR91; TCA cycle; atherosclerosis; citrate; fumarate; itaconate; succinate.

MeSH terms

Atherosclerosis* / metabolism
Citric Acid Cycle*
Energy Metabolism
Humans
Inflammation / metabolism
Macrophages / metabolism

Abstract

MeSH terms

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