Smoking and the Pathophysiology of Peripheral Artery Disease

Wang, Weiming; Zhao, Tingting; Geng, Kang; Yuan, Gang; Chen, Yue; Xu, Youhua

doi:10.3389/fcvm.2021.704106

Cited by 43 publications

(37 citation statements)

References 194 publications

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“…The identification of the multitude of loci and genes of susceptibility to LEAD and the combination of them, constitutes a challenge for future research. Smoking is considered an environmental factor with a major risk for LEAD, but the different susceptibility to LEAD in the case of smokers suggests that the interaction with genetic factors can influence the evolution and progression of LEAD [ 18 , 22 , 93 ].…”

Section: Discussion and Future Challengesmentioning

confidence: 99%

“…Previous studies have focused on analyzing the association between smoking [ 93 , 94 ] and obesity [ 94 ], with susceptibility loci for LEAD [ 93 , 94 ]. In the future, studying the association between DM, ESRD, and LEAD could shed light on the still unknown aspects of the pathophysiological mechanisms of LEAD [ 22 ].…”

Section: Discussion and Future Challengesmentioning

confidence: 99%

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The Genetic Architecture of the Etiology of Lower Extremity Peripheral Artery Disease: Current Knowledge and Future Challenges in the Era of Genomic Medicine

Butnariu

Gorduza

Florea

et al. 2022

IJMS

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Lower extremity artery disease (LEAD), caused by atherosclerotic obstruction of the arteries of the lower limb extremities, has exhibited an increase in mortality and morbidity worldwide. The phenotypic variability of LEAD is correlated with its complex, multifactorial etiology. In addition to traditional risk factors, it has been shown that the interaction between genetic factors (epistasis) or between genes and the environment potentially have an independent role in the development and progression of LEAD. In recent years, progress has been made in identifying genetic variants associated with LEAD, by Genome-Wide Association Studies (GWAS), Whole Exome Sequencing (WES) studies, and epigenetic profiling. The aim of this review is to present the current knowledge about the genetic factors involved in the etiopathogenic mechanisms of LEAD, as well as possible directions for future research. We analyzed data from the literature, starting with candidate gene-based association studies, and then continuing with extensive association studies, such as GWAS and WES. The results of these studies showed that the genetic architecture of LEAD is extremely heterogeneous. In the future, the identification of new genetic factors will allow for the development of targeted molecular therapies, and the use of polygenic risk scores (PRS) to identify individuals at an increased risk of LEAD will allow for early prophylactic measures and personalized therapy to improve their prognosis.

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Section: Discussion and Future Challengesmentioning

confidence: 99%

Section: Discussion and Future Challengesmentioning

confidence: 99%

The Genetic Architecture of the Etiology of Lower Extremity Peripheral Artery Disease: Current Knowledge and Future Challenges in the Era of Genomic Medicine

Butnariu

Gorduza

Florea

et al. 2022

IJMS

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“…Both immunosenescence and atherosclerosis are multifactorial conditions which share common stimulators, including Ox-LDL ( 111 , 112 ), inflammation ( 113 , 114 ), ROS ( 115 , 116 ), cigarette smoke ( 117 , 118 ), hypertension ( 119 , 120 ), hyperglycaemia ( 121 , 122 ), viral infection ( 123 , 124 ), mitochondrial failure ( 125 , 126 ) and genomic damage ( 127 , 128 ) ( Figure 1 ). Certainly, various drivers of senescence induce SASP secretion and thereby stimulate chronic and low-grade inflammation that participates in atherosclerosis development, and in turn, diverse stimulators of atherosclerosis induce cellular senescence and SASP production.…”

Section: Drivers Of Immunosenescence and Atherosclerosismentioning

confidence: 99%

Immunosenescence in atherosclerosis: A role for chronic viral infections

Talepoor

Doroudchi

2022

Front. Immunol.

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Immune system is a versatile and dynamic body organ which offers survival and endurance of human beings in their hostile living environment. However, similar to other cells, immune cells are hijacked by senescence. The ageing immune cells lose their beneficial functions but continue to produce inflammatory mediators which draw other immune and non-immune cells to the senescence loop. Immunosenescence has been shown to be associated with different pathological conditions and diseases, among which atherosclerosis has recently come to light. There are common drivers of both immunosenescence and atherosclerosis; e.g. inflammation, reactive oxygen species (ROS), chronic viral infections, genomic damage, oxidized-LDL, hypertension, cigarette smoke, hyperglycaemia, and mitochondrial failure. Chronic viral infections induce inflammaging, sustained cytokine signaling, ROS generation and DNA damage which are associated with atherogenesis. Accumulating evidence shows that several DNA and RNA viruses are stimulators of immunosenescence and atherosclerosis in an interrelated network. DNA viruses such as CMV, EBV and HBV upregulate p16, p21 and p53 senescence-associated molecules; induce inflammaging, metabolic reprogramming of infected cells, replicative senescence and telomere shortening. RNA viruses such as HCV and HIV induce ROS generation, DNA damage, induction of senescence-associated secretory phenotype (SASP), metabolic reprogramming of infected cells, G1 cell cycle arrest, telomere shortening, as well as epigenetic modifications of DNA and histones. The newly emerged SARS-CoV-2 virus is also a potent inducer of cytokine storm and SASP. The spike protein of SARS-CoV-2 promotes senescence phenotype in endothelial cells by augmenting p16, p21, senescence-associated β-galactosidase (SA-β-Gal) and adhesion molecules expression. The impact of SARS-CoV-2 mega-inflammation on atherogenesis, however, remains to be investigated. In this review we focus on the common processes in immunosenescence and atherogenesis caused by chronic viral infections and discuss the current knowledge on this topic.

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“…Banyak studi telah menunjukkan bahwa merokok merupakan faktor risiko independen terhadap PAP. Seseorang yang sudah lama merokok selama kurang dari 25 tahun mempunyai 3 kali lipat peningkatan resiko berkembangnya PAP dibandingkan tidak perokok, sedangkan seseorang yang telah merokok selama 25 tahun atau lebih memiliki resiko peningkatan 5 kali lipat (5).…”

Section: Abstrakunclassified

Karakteristik Klinis dan Skor Ankle Brachial Index (ABI) Pada Lansia di Panti Sosial Tresna Werdha Budi Mulia 3 Jakarta Selatan

Renovaldi

Afrijiyah

2022

MuJG

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Latar belakang: Lansia adalah seseorang yang sudah memasuki usia 60 tahun keatas. Lansia rentan mengalami beberapa masalah kesehatan vaskular seperti, hipertensi, stroke, diabetes melitus dan jantung koroner yang terpengaruh oleh keterlambatan regeneratif yaitu fisik, kognitif bahkan emosional. Salah satu metode untuk mendeteksi gangguan ini adalah Ankle Brachial Index (ABI). Ankle Brachial Index (ABI) adalah metode yang direkomendasikan untuk diagnosis penyakit arteri perifer (PAP), yakni penyakit yang menyebabkan gangguan aliran darah pada ekstremitas yang biasanya disebabkan oleh aterosklerosis. Tujuan: Penelitian. Diketahuinya karakteristik klinis dan skor Ankle Brachial Index (ABI) pada Lansia di Panti Sosial Tresna Werdha Budi Mulia 3. Metode: Penelitian ini merupakan penelitian kuantitatif yang bersifat observasional analitik dengan pendekatan cross sectional. Penelitian ini dilakukan untuk mengetahui hubungan karakteristik klinis dengan skor ABI pada lansia dengan jumlah sampel sebanyak 60 responden. Hasil: Hasil penelitian menyatakan bahwa terdapat hubungan bermakna antara indeks massa tubuh (IMT) dan riwayat komorbid terhadap skor ABI pada lansia dengan nilai p pada IMT (p=0.002) dan nilai p pada riwayat komorbid (p=0.000). namun tidak terdapat hubungan bermakna antara usia, jenis kelamin, dan riwayat merokok dengan skor Ankle Brachial Index (ABI) pada lansia dengan nilai (p= >0,05). Simpulan: Mayoritas lansia di Panti Sosial Tresna Budi Mulia 3 memiliki skor Ankle Brachial Index (ABI) yang normal. Tidak terdapat hubungan bermakna antara usia, jenis kelamin, dan riwayat merokok dengan skor Ankle Brachial Index (ABI), namun terdapat hubungan bermakna antara indeks massa tubuh (IMT) dan riwayat komorbid terhadap skor ABI.

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Smoking and the Pathophysiology of Peripheral Artery Disease

Cited by 43 publications

References 194 publications

The Genetic Architecture of the Etiology of Lower Extremity Peripheral Artery Disease: Current Knowledge and Future Challenges in the Era of Genomic Medicine

The Genetic Architecture of the Etiology of Lower Extremity Peripheral Artery Disease: Current Knowledge and Future Challenges in the Era of Genomic Medicine

Immunosenescence in atherosclerosis: A role for chronic viral infections

Karakteristik Klinis dan Skor Ankle Brachial Index (ABI) Pada Lansia di Panti Sosial Tresna Werdha Budi Mulia 3 Jakarta Selatan

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