PM2.5 aggravates the lipid accumulation, mitochondrial damage and apoptosis in macrophage foam cells

Liu, Jiangyan; Liang, Shuang; Du, Zhou; Zhang, Jingyi; Sun, Baiyang; Zhao, Tong; Yang, Xiaozhe; Shi, Yanfeng; Duan, Junchao; Sun, Zhiwei

doi:10.1016/j.envpol.2019.03.045

Cited by 62 publications

(23 citation statements)

References 51 publications

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“…Researches have fully indicated that PM2.5 may trigger cell death, including autophagy, necrosis and apoptosis [9][10][11]. Not only that, PM2.5 related pyroptosis and ferroptosis is also been explore in this review.…”

Section: Introductionmentioning

confidence: 85%

“…And they also demonstrated that mitochondria-mediated apoptosis pathway played a critical role in PM-induced myocardial cytotoxicity in AC16 contributing to cardiac dysfunction [32]. As is also in myocardial cells, they found that PM2.5 aggravated mitochondrial damage, lipid accumulation and apoptosis in macrophage foam cells to induce atherosclerotic plaque progression [10]. Apart from Prof. Sun's researches, Xu et al found that PM2.5 exposure induced serious bad effects shown as inflammation and oxidative stress in hyperlipidemic rats, then triggered cardiomyocyte apoptosis by caspase3 through JNK/P53 pathway [33].…”

Section: Pm25 and Apoptosismentioning

confidence: 92%

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PM2.5-related cell death patterns

Wang¹,

Zhong²,

Liao³

et al. 2021

Int. J. Med. Sci.

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With the increasingly serious problem of environmental pollution, the health problems caused by PM2.5 are gradually coming into our line of sight. Previous researches have indicated that air pollution is nearly related to various diseases, but few studies have focused on the exact function mediated by particulate matter less than 2.5 (PM2.5) in these diseases. PM2.5 is known to induce multiple ways of cell death, including autophagy, necrosis, apoptosis, pyroptosis and ferroptosis. Therefore, it is of much importance to understand the different ways of cell death caused by PM2.5 in the pathogenesis and treatment of PM2.5-related diseases. This present review is an insight of multiple ways of PM2.5-induced cell death in different diseases.

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Section: Introductionmentioning

confidence: 85%

Section: Pm25 and Apoptosismentioning

confidence: 92%

PM2.5-related cell death patterns

Wang¹,

Zhong²,

Liao³

et al. 2021

Int. J. Med. Sci.

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“…5). ROS increase, Ca 2+ influx, and severe mitochondrial dysfunction could lead to Cyt C release from mitochondria into the cytoplasm (Liu et al 2018a;Liu et al 2019). Then, Cyt C and caspase-9 form apoptotic bodies, activate caspase-3, thereby leading to cellular apoptosis (Scorrano and Korsmeyer 2003).…”

Section: Discussionmentioning

confidence: 99%

Cytotoxicity induced by fine particulate matter (PM2.5) via mitochondria-mediated apoptosis pathway in rat alveolar macrophages

Wei

Yuan

et al. 2021

Environ Sci Pollut Res

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Although positive associations exist between ambient particulate matter (PM 2.5 ; diameter ≤ 2.5 μm) and the morbidity and mortality rates for respiratory diseases, the biological mechanisms of the reported health effects are unclear. Considering that alveolar macrophages (AM) are the main cells responsible for phagocytic clearance of xenobiotic particles that reach the airspaces of the lungs, the purpose of this study was to investigate whether PM 2.5 induced AM apoptosis, and investigate its possible mechanisms. Freshly isolated AM from Wistar rats were treated with extracted PM 2.5 at concentrations of 33, 100, or 300 μg/mL for 4 h; thereafter, the cytotoxic effects were evaluated. The results demonstrated that PM 2.5 induced cytotoxicity by decreasing cell viability and increasing lactate dehydrogenase (LDH) levels in AMs. The levels of reactive oxygen species (ROS) and intracellular calcium cations (Ca 2+) markedly increased in higher PM 2.5 concentration groups. Additionally, the apoptotic ratio increased, and the apoptosis-related proteins BCL2-associated X (Bax), caspase-3, and caspase-9 were upregulated, whereas B cell lymphoma-2 (Bcl-2) protein levels were downregulated following PM 2.5 exposure. Cumulative findings showed that PM 2.5 induced apoptosis in AMs through a mitochondrial-mediated pathway, which indicated that PM 2.5 plays a significant role in lung injury diseases.

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“…Oxidized low-density lipoprotein (ox-LDL) primes and activates the NOD-like receptor protein 3 (NLRP3) inflammasome by binding to TLR4 or CD36 in macrophages and increases the release of inflammatory cytokines (IL-1β and IL-18) and pyroptosis [11]. PM 2.5 induces oxidative stress, increasing the apoptosis of foam cells via the mitochondrial apoptosis pathway [52]. PM 2.5 impairs HDL functions such as HDL-mediated cholesterol efflux, thus facilitating foam cell formation and accumulation [53].…”

Section: Pm 25 and Atherosclerosismentioning

confidence: 99%

“…Moreover, in ApoE -/mice exposed to a mixture of gasoline and diesel engine exhaust (MVE), the expression of LOX-1 was increased in cerebral microvascular endothelial cells, and at least in part, MVE altered the structure and integrity of the brain microvasculature via LOX-1 signaling [176]. Many studies have demonstrated that PM 2.5 contributes to lipid dysregulation in the sera of ApoE -/mice and promotes macrophage engulfment of ox-LDL through surface scavenger receptors to induce foam cell formation [6,12,177]. However, studies on the effect of PM 2.5 on lipid uptake and transport in endothelial cells are lacking, although limited evidence has shown that traffic-derived pollutants increase LOX-1 signaling in endothelial cells.…”

Section: Ambient Pm 25 Promotes Lipid Depositionmentioning

confidence: 99%

The critical role of endothelial function in fine particulate matter-induced atherosclerosis

et al. 2020

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Ambient and indoor air pollution contributes annually to approximately seven million premature deaths. Air pollution is a complex mixture of gaseous and particulate materials. In particular, fine particulate matter (PM2.5) plays a major mortality risk factor particularly on cardiovascular diseases through mechanisms of atherosclerosis, thrombosis and inflammation. A review on the PM2.5-induced atherosclerosis is needed to better understand the involved mechanisms. In this review, we summarized epidemiology and animal studies of PM2.5-induced atherosclerosis. Vascular endothelial injury is a critical early predictor of atherosclerosis. The evidence of mechanisms of PM2.5-induced atherosclerosis supports effects on vascular function. Thus, we summarized the main mechanisms of PM2.5-triggered vascular endothelial injury, which mainly involved three aspects, including vascular endothelial permeability, vasomotor function and vascular reparative capacity. Then we reviewed the relationship between PM2.5-induced endothelial injury and atherosclerosis. PM2.5-induced endothelial injury associated with inflammation, pro-coagulation and lipid deposition. Although the evidence of PM2.5-induced atherosclerosis is undergoing continual refinement, the mechanisms of PM2.5-triggered atherosclerosis are still limited, especially indoor PM2.5. Subsequent efforts of researchers are needed to improve the understanding of PM2.5 and atherosclerosis. Preventing or avoiding PM2.5-induced endothelial damage may greatly reduce the occurrence and development of atherosclerosis.

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PM2.5 aggravates the lipid accumulation, mitochondrial damage and apoptosis in macrophage foam cells

Cited by 62 publications

References 51 publications

PM2.5-related cell death patterns

PM2.5-related cell death patterns

Cytotoxicity induced by fine particulate matter (PM2.5) via mitochondria-mediated apoptosis pathway in rat alveolar macrophages

The critical role of endothelial function in fine particulate matter-induced atherosclerosis

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