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논문 기본 정보

자료유형
학술저널
저자정보
Kai Wen Wai (School of Biosciences, Taylor’s University, Subang Jaya, Selangor Darul Ehsan, Malaysia.) Liang Ee Low (Chemical Engineering Discipline, School of Engineering, Monash University Malaysia, Jalan Lagoon Selatan, Bandar Sunway, Subang Jaya, Selangor, Malaysia.Monash-Industry Plant Oils Research L) Bey Hing Goh (Biofunctional Molecule Exploratory Research Group, School of Pharmacy, Monash University Malaysia, Bandar Sunway, Selangor Darul Ehsan, Malaysia.Department of Biological Sciences, School of) Wei Hsum Yap (School of Biosciences, Taylor’s University, Subang Jaya, Selangor Darul Ehsan, Malaysia.)
저널정보
한국지질동맥경화학회(구 한국지질학회) 지질·동맥경화학회지 Journal of Lipid and Atherosclerosis Vol.13 No.3
발행연도
2024.9
수록면
292 - 305 (14page)
DOI
10.12997/jla.2024.13.3.292

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Nuclear factor erythroid 2-related factor 2 (Nrf2), a transcriptional factor that maintains intracellular redox equilibrium, modulates the expression of antioxidant genes, scavenger receptors, and cholesterol efflux transporters, all of which contribute significantly to foam cell development and plaque formation. Nrf2 has recently emerged as a key regulator that connects autophagy and vascular senescence in atherosclerosis. Autophagy, a cellular mechanism involved in the breakdown and recycling of damaged proteins and organelles, and cellular senescence, a state of irreversible growth arrest, are both processes implicated in the pathogenesis of atherosclerosis. The intricate interplay of these processes has received increasing attention, shedding light on their cumulative role in driving the development of atherosclerosis. Recent studies have revealed that Nrf2 plays a critical role in mediating autophagy and senescence in atherosclerosis progression. Nrf2 activation promotes autophagy, which increases lipid clearance and prevents the development of foam cells. Meanwhile, the activation of Nrf2 also inhibits cellular senescence by regulating the expression of senescence markers to preserve cellular homeostasis and function and delay the progression of atherosclerosis. This review provides an overview of the molecular mechanisms through which Nrf2 connects cellular autophagy and vascular senescence in atherosclerosis. Understanding these mechanisms can provide insights into potential therapeutic strategies targeting Nrf2 to modulate cellular autophagy and vascular senescence, thereby preventing the progression of atherosclerosis.

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