The role of p53 in the alternation of vascular functions

Chan, Gloria; Chan, Enoch; Kwok, Carsten Tsun-Ka; Leung, George Pak‐Heng; Lee, Simon Ming‐Yuen; Seto, Sai Wang

doi:10.3389/fphar.2022.981152

Cited by 16 publications

(10 citation statements)

References 98 publications

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“… 53 Furthermore, NLRC3 deficiency promotes cutaneous wound healing due to the inhibition of p53 signaling. 54 As p53 is also involved in vascular remodeling and atherosclerosis, 55 thus we speculate that NLRC3 alteration could have reversed the expression and phosphorylation of p53 that is usually observed in advanced atherosclerotic plaques 56 and therefore reduced restenosis susceptibility. Further studies are needed to explore this relationship.…”

Section: Discussionmentioning

confidence: 92%

Genetic Variants in PHACTR1 & LPL Mediate Restenosis Risk in Coronary Artery Patients

Hageh¹,

Chacar²,

Venkatachalam³

et al. 2023

VHRM

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Background and Objective Coronary artery disease (CAD) is a major cause of death worldwide. Revascularization via stent placement or coronary artery bypass grafting (CABG) are standard treatments for CAD. Despite a high success rate, these approaches are associated with long-term failure due to restenosis. Risk factors associated with restenosis were investigated using a case-control association study design. Methods Five thousand two hundred and forty-two patients were enrolled in this study and were assigned as follows: Stenosis Group: 3570 patients with CAD >50% without a prior stent or CABG (1394 genotyped), and Restenosis Group: 1672 patients with CAD >50% and prior stent deployment or CABG (705 genotyped). Binomial regression models were applied to investigate the association of restenosis with diabetes, hypertension, and dyslipidemia. The genetic association with restenosis was conducted using PLINK 1.9. Results Dyslipidemia is a major risk factor (Odds Ratio (OR) = 2.14, P-value <0.0001) for restenosis particularly among men (OR = 2.32, P < 0.0001), while type 2 diabetes (T2D) was associated with an increased risk of restenosis in women (OR = 1.36, P = 0.01). The rs9349379 ( PHACTR1) and rs264 ( LPL ) were associated with an increased risk of restenosis in our patients. PHACTR1 variant was associated with increased risk of restenosis mainly in women and in diabetic patients, while the LPL variant was associated with increased risk of restenosis in men. Conclusion The rs9349379 in PHACTR1 gene is significantly associated with restenosis, this association is more pronounced in women and in diabetic patients. The rs264 in LPL gene was associated with increased risk of restenosis in male patients.

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Section: Discussionmentioning

confidence: 92%

Genetic Variants in PHACTR1 & LPL Mediate Restenosis Risk in Coronary Artery Patients

Hageh¹,

Chacar²,

Venkatachalam³

et al. 2023

VHRM

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“…Finally, long-term PM 2.5 and PM 10 exposures were associated with higher levels of alpha-1 antitrypsin [ 86 ]. Given the role of p53 signaling in anti-angiogenesis, programmed cell death, metabolism regulation, and vasodilation, this pathway can affect cardiovascular outcomes [ 242 , 243 ]. In addition, p53 signaling plays a supportive role in the maintenance of lung homeostasis; therefore, dysregulation and deficiency of p53 signaling can be associated with respiratory diseases [ 244 ].…”

Section: Resultsmentioning

confidence: 99%

Methylomic, Proteomic, and Metabolomic Correlates of Traffic-Related Air Pollution in the Context of Cardiorespiratory Health: A Systematic Review, Pathway Analysis, and Network Analysis

Casella,

Kiles,

Urquhart

et al. 2023

Toxics

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A growing body of literature has attempted to characterize how traffic-related air pollution (TRAP) affects molecular and subclinical biological processes in ways that could lead to cardiorespiratory disease. To provide a streamlined synthesis of what is known about the multiple mechanisms through which TRAP could lead to cardiorespiratory pathology, we conducted a systematic review of the epidemiological literature relating TRAP exposure to methylomic, proteomic, and metabolomic biomarkers in adult populations. Using the 139 papers that met our inclusion criteria, we identified the omic biomarkers significantly associated with short- or long-term TRAP and used these biomarkers to conduct pathway and network analyses. We considered the evidence for TRAP-related associations with biological pathways involving lipid metabolism, cellular energy production, amino acid metabolism, inflammation and immunity, coagulation, endothelial function, and oxidative stress. Our analysis suggests that an integrated multi-omics approach may provide critical new insights into the ways TRAP could lead to adverse clinical outcomes. We advocate for efforts to build a more unified approach for characterizing the dynamic and complex biological processes linking TRAP exposure and subclinical and clinical disease and highlight contemporary challenges and opportunities associated with such efforts.

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“…Aging is a major risk factor for many diseases including atherosclerosis [ 7 , 29 , 30 ]. Senescent endothelial cells have been found in atherosclerotic plaques in elderly patients, and endothelial cell senescence is considered a potential pathophysiological factor in the development of cardiovascular disease [ 21 , 31 , 32 ]. This study is the first to demonstrate that RRP can attenuate H 2 O 2 -induced cellular senescence in HAECs by inducing autophagy via the activation of the AMPK signaling pathway.…”

Section: Discussionmentioning

confidence: 99%

RRP Regulates Autophagy through the AMPK Pathway to Alleviate the Effect of Cell Senescence on Atherosclerosis

Liu

Song

et al. 2023

Oxidative Medicine and Cellular Longevity

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Autophagy is closely associated with atherosclerosis and other cardiovascular diseases (CVD). Compound Danshen prescription is widely used as a clinical antiatherosclerotic drug. In our previous studies, we have shown that the combined active component, ginsenoside Rg1-notoginsenoside R1-protocatechualdehyde (RRP), can effectively alleviate endothelial dysfunction and reduce atherosclerotic plaques. However, the association between cellular senescence, caused by reduced autophagy, and atherosclerosis remains unclear. In this study, we investigated whether RRP can enhance autophagy and alleviate cell senescence through the AMPK pathway. Our results showed that RRP reduced the secretion of inflammatory factors in the serum of atherosclerotic mice, enhanced autophagy, and alleviated aortic aging in mice, thus reducing atherosclerotic plaques. In human aortic endothelial cells (HAECs), RRP effectively enhanced autophagy and inhibited senescence by activating the AMPK pathway. When AMPKα was silenced, the effect of RRP was inhibited, thus reversing its antiaging effect. Overall, our results show that RRP regulates autophagy through the AMPK pathway, thereby inhibiting cell senescence and alleviating the progression of atherosclerosis, suggesting that RRP may be a potential candidate drug for the treatment of atherosclerosis.

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The role of p53 in the alternation of vascular functions

Cited by 16 publications

References 98 publications

Genetic Variants in PHACTR1 & LPL Mediate Restenosis Risk in Coronary Artery Patients

Genetic Variants in PHACTR1 & LPL Mediate Restenosis Risk in Coronary Artery Patients

Methylomic, Proteomic, and Metabolomic Correlates of Traffic-Related Air Pollution in the Context of Cardiorespiratory Health: A Systematic Review, Pathway Analysis, and Network Analysis

RRP Regulates Autophagy through the AMPK Pathway to Alleviate the Effect of Cell Senescence on Atherosclerosis

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