Abstract
Atherosclerosis is a leading cause of cardiovascular diseases (CVD) worldwide and intimately linked to aging. This pathology is characterized by chronic inflammation, oxidative stress, gradual accumulation of low-density lipoproteins (LDL) particles and fibrous elements in focal areas of large and medium arteries. These fibrofatty lesions in the artery wall become progressively unstable and thrombogenic leading to heart attack, stroke or other severe heart ischemic syndromes. Elevated blood levels of LDL are major triggering events for atherosclerosis. A cascade of molecular and cellular events results in the atherosclerotic plaque formation, evolution, and rupture. Moreover, the senescence of multiple cell types present in the vasculature were reported to contribute to atherosclerotic plaque progression and destabilization. Classical therapeutic interventions consist of lipid-lowering drugs, anti-inflammatory and life style dispositions. Moreover, targeting oxidative stress by developing innovative antioxidant agents or boosting antioxidant systems is also a well-established strategy. Accumulation of senescent cells (SC) is also another important feature of atherosclerosis and was detected in various models. Hence, targeting SCs appears as an emerging therapeutic option, since senolytic agents favorably disturb atherosclerotic plaques. In this review, we propose a survey of the impact of inflammation, oxidative stress, and senescence in atherosclerosis; and the emerging therapeutic options, including thioredoxin-based approaches such as anti-oxidant, anti-inflammatory, and anti-atherogenic strategy with promising potential of senomodulation.
Highlights
Accepted: 19 December 2021Cardiovascular diseases (CVDs), principally ischemic heart disease and stroke, are the leading cause of global mortality and a major contributor to disability
ATP-binding cassette transporters ABCA1 and ABCG1 and the scavenger receptor scavenger receptors (SR)-BI. This regulation of cholesterol metabolism is altered in atherosclerosis; in this sense, foam cells are the result of an unregulated accumulation of oxidized LDL (oxLDL) and cholesterol esters within the macrophages located in the intima in response to activated endothelial cells (EC) by inflammation
We previously demonstrated that one Thioredoxin mimetic peptides (TxMPs), CB3, exerts vasculo-protective effects, by reducing inflammation, oxidative stress, NF-κB activation, M1 macrophage orientation, and surfaces of atherosclerotic lesions in ApoE2.Ki mice [221]
Summary
Cardiovascular diseases (CVDs), principally ischemic heart disease and stroke, are the leading cause of global mortality and a major contributor to disability. The CVDs are often complications of atherosclerosis, characterized by the formation of fibrofatty lesions in the artery wall that begins early in life and progresses gradually, remaining usually asymptomatic for a long period of time [2]. Atherosclerosis is a disease characterized by low-grade, chronic inflammation of the arterial wall. The risk factors for CVD can be either non-modifiable; such as age, gender, ethnicity, and genetics; or modifiable, such as elevated serum lipids, high blood pressure, high fasting plasma glucose, high LDL-cholesterol, low physical activity, obesity, ambient and household air pollution, and tobacco [1,4,5]. We highlight the roles of thioredoxine-1 system as an endogenous resolution mediator in suppressing atherogenic processes and how this system might be used as a therapy to prevent atherosclerotic cardiovascular diseases
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