From: The critical role of endothelial function in fine particulate matter-induced atherosclerosis
Reference | PM2.5 source | Mouse model | Diet | Exposure Time | Findings |
---|---|---|---|---|---|
[94] | Shanghai, China Ambient PM2.5 | ApoE-/- mice | Normal chow; High-fat diet | 8 h/day, 7 days/week, 16 weeks | PM2.5 exposure induced and promoted atherosclerotic lesions with significant difference. Increased: Atherosclerotic plaque; lipids (ApoB, LDL-C, T-CHO, TG); CD36; ox-LDL; inflammatory cytokines (IL-1β, IL-18); NLRP3, caspase-1, ASC, pro-caspase-1, cleaved-caspase-1; Decreased: Lipids (ApoA1 and HDL-C) |
[95] | Nanjing, China Ambient PM2.5 | ApoE-/- mice | High-fat diet | 12 weeks | PM2.5 exposure amplified atherosclerotic lesions with significant difference. Increased: Atherosclerotic plaque; lipid accumulation; TC; LDL-C; Inflammatory cytokines (IL-6, TNF-α); Deceased: Anti-inflammatory cytokines (IL-10, TGF-β); CD4+CD25+Foxp3+Tregs; Foxp3 |
[96] | Beijing, China Ambient PM (PM2.5 and PM10) | ApoE-/- mice | High-fat diet | 24 h/day, 7 days/week, 2 months | PM2.5 increased atherosclerotic plaque with significant difference. Increased: Lesion area; TC; LDL; ox-LDL; visfatin; systemic inflammation and pulmonary inflammation response (IL-6, TNF-α); MDA Decreased: SOD; GSH-Px |
[97] | Beijing, China Ambient PM (PM2.5 and PM10) | ApoE-/- mice | High-fat diet | 24 h/day, 7 days/week, 2 months | PM2.5 exposure increased atherosclerotic plaque with significant difference. Increased: Plaque area; TC; LDL; ox-LDL; systemic inflammation (Hs-CRP, IL-6, TNF-α) and pulmonary inflammation response (IL-6, TNF-α); Decreased: T-AOC; SOD |
[12] | Michigan State University, USA Ambient PM2.5 | ApoE-/- or LDLR-/- mice | High-fat diet | 6 h/day, 5 days/week, 6 months | PM2.5 exposure increased atherosclerotic plaque with significant difference. Increased: Lesion area; lipid and collagen content; 7-KCh and uptake; CD36; foam cell formation |
[51] | Nanjing, China Ambient PM2.5 | ApoE-/- mice | High-fat diet | twice/week, 12 weeks or 24 weeks | PM2.5 exposure promoted atherosclerotic plaque development and increased plaque vulnerability, with significant difference. Increased: Lesion area, lipid; broken aortic elastic fibers; Decreased: Collagen content; fibrous cap |
[6] | Beijing, China Ambient PM2.5 | ApoE-/- mice | High-fat diet | Every 3 days, 2 months, | PM2.5 exposure increased the formation of atherosclerosis and the influence probably persisted after 1-month recovery, with significant difference. Increased: Atherosclerotic lesion; inflammatory cytokines; lipid metabolism alteration. |
[98] | Tianjin, China Traffic related PM2.5, simulated PM2.5 | ApoE-/- mice | High-fat diet | Every two days, 10 weeks | Traffic related and simulated PM2.5 promoted the formation of atherosclerosis with significant difference. Increased: Plaque; T-CHO; LDL-C; TG; MDA; Decreased: HDL-C; SOD; GSH-Px |
[99] | Northeastern, China Ambient PM2.5, WDE, DEG | ApoE-/- mice | Normal chow | average of 5.2 hours/day, 4 days/week, 3 months and 5 months | Exposure to PM2.5 for 5 months induced atherosclerotic plaques with significant difference. For plaque exacerbation, PM2.5 > WDE > DEG = FA Increased: Plaque; vasomotor dysfunction; inflammation |
[100] | Yinchuan, China coal-fired PM2.5 | C57BL/6J mice and ApoE-/- mice | High-fat diet | 3 h/day, 1 day/week, 8 weeks | Coal-fired PM2.5 significantly promoted the formation atherosclerosis with significant difference. Increased: Plaque; foam cells; fibrous cap formation; ET-1; ICAM-1; E-selectin Decreased: vWF |
[101] | Manhattan, USA PM2.5 | ApoE-/- mice | Normal chow and High-fat diet | 6 h/day, 5 day/week, 6 months | In high-fat diet group, PM2.5 increased plaque area compared with FA (p < 0.01); In normal chow group, PM2.5 increased plaque area compared with FA (p < 0.15). Increased: Plaque area; Cholesterol; Constriction response; CD68; 3-Nitrotyrosine; eNOS; iNOS; Decreased: Relaxation response |
[102] | Los Angeles freeway, USA PM2.5 | ApoE-/- mice | regular diet | 5 h/day, 3 day/week, 75 hours | PM2.5 resulted in aortic atherosclerotic lesion increased trend (p = 0.1). Increased: Plaque area; Liver MDA; Decreased: HDL anti-inflammatory properties |
[103] | New York; USA PM2.5 | C57BL/6, ApoE-/- mice, ApoE and LDLR double knockout (DK) | High-fat diet and regular diet | 6 h/day, 5 day/week, 5 months | PM2.5 exposure increased atherosclerotic lesion in ApoE-/- mice (p < 0.05). Atherosclerotic lesion 57% increase in ApoE-/- mice; Atherosclerotic lesion 10% increase in male DK mice and 8% decrease in female DK mice. |
[104] | New York; USA PM2.5 | ApoE-/- mice | High-fat diet | 30 mg/kg/day, 8 weeks | PM2.5 contributed to the progression of atherosclerosis (p < 0.05). Increased: Atherosclerotic plaques; numbers of lesion macrophages; endothelial layer injury; platelets and leukocytes adherence; IL-6; TNF-α; iNOS; IL-12; arginase-1; CD206 |
[26] | DEP, 1650b, NIST, USA | C57BL/6, ApoE-/- mice | Regular chow or high-fat diet | Once a day during 5 days/week, 3-6 weeks | DEP exposure increased atherosclerotic lesion in ApoE-/- mice (p < 0.05). Increased: Atherosclerotic plaques; EPC apoptosis; superoxide production; Decreased: Neoangiogenesis; EPC migration; Endothelial cell interity |
[25] | DEP, SRM-2975, NIST, USA | C57BL/6, ApoE-/- mice | Regular chow or high-fat diet | Twice weekly instillation | DEP exposure increased atherosclerotic lesion in ApoE-/- mice (p < 0.05). Increased: Atherosclerotic plaques; Cholesterol; antioxidant genes in the liver |