Nicotine in Senescence and Atherosclerosis

Centner, Ann; Bhide, Pradeep G.; Salazar, Gloria

doi:10.3390/cells9041035

Cited by 48 publications

(20 citation statements)

References 234 publications

(290 reference statements)

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“…The impact of nicotine exposure on the cardiovascular system is complex, from its modulation of autonomic function to its direct effects on individual cell types in the vasculature. Although the initial presentations of nicotine‐induced vascular dysfunction may be insidious (changes in vasoreactivity and vascular remodelling as discussed in this review), these changes contribute to the pathogenesis of serious medical conditions including atherosclerosis, abdominal aortic aneurysm, coronary artery disease and myocardial infarction 123–125 …”

Section: Discussionmentioning

confidence: 99%

“…Although the initial presentations of nicotine-induced vascular dysfunction may be insidious (changes in vasoreactivity and vascular remodelling as discussed in this review), these changes contribute to the pathogenesis of serious medical conditions including atherosclerosis, abdominal aortic aneurysm, coronary artery disease and myocardial infarction. [123][124][125] Nicotine has been studied for over 50 years; however, our understanding of the impact of nicotine on cardiovascular function and its associated mechanisms is far from complete. In terms of nicotine-induced vascular dysfunction, most studies have implicated the involvement of α7-nAChR; however, investigation into other nAChR that could play important roles in the vascular effects of nicotine is needed.…”

Section: Directionsmentioning

confidence: 99%

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Nicotine and vascular dysfunction

2021

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Cigarette smoking is the single most important risk factor for the development of cardiovascular diseases (CVDs). However, the role of nicotine, the addictive component of all tobacco products, in the development of CVD is incompletely understood. Although increased public awareness of the harms of cigarette smoking has successfully led to a decline in its prevalence, the use of electronic cigarettes (e‐cig) or electronic nicotine delivery system has increased dramatically in recent years because of the perception that these products are safe. This review summarizes our current knowledge of the expression and function of the nicotinic acetylcholine receptors in the cardiovascular system and the impact of nicotine exposure on cardiovascular health, with a focus on nicotine‐induced vascular dysfunction. Nicotine alters vasoreactivity through endothelium‐dependent and/or endothelium‐independent mechanisms, leading to clinical manifestations in both cigarette smokers and e‐cig users. In addition, nicotine induces vascular remodelling through its effects on proliferation, migration and matrix production of both vascular endothelial and vascular smooth muscle cells. The purpose of this review is to identify critical knowledge gaps regarding the effects of nicotine on the vasculature and to stimulate continued nicotine research.

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Section: Discussionmentioning

confidence: 99%

Section: Directionsmentioning

confidence: 99%

Nicotine and vascular dysfunction

2021

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“…Greater effects of aging on cerebrovascular morphologies in smokers were observed in this study. A previous report has indicated that cigarette smoking could induce vascular smooth muscle cell senescence (Centner, Bhide and Salazar 2020). The accumulation of senescent VSMCs with aging may be the underlying cause for our observation.…”

Section: Discussionmentioning

confidence: 99%

Morphological alternations of intracerebral arterial during middle age: a community cohort study

Zhang

Yang

et al. 2021

Preprint

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Background Ample evidence has suggested that vascular modifications are associated with aging. To expand previous understanding of age-related vascular changes, we examined the association between aging and cerebrovascular morphologies.Methods1176 participants aged 35 to 75 years recruited from Shanghai, China were included in this study. Cerebrovascular morphological features comprising arterial branch density, radius, and tortuosity were quantified using three-dimensional magnetic resonance angiography. Linear regression was used to examine the association between age and vasculature features.ResultsAge was found to be a significant predictor for cerebrovascular morphological alterations after adjusting for vascular risk factors. However, after dividing subjects into subgroups based on their age, aging was found to be significantly correlated with all three morphometric features only in the 45-54 subgroup after adjusting for the other vascular risk factors. Smoking gives rise to a more rapid age-related changes in vascular morphologies, while alcohol consumption could decelerate those age-related alterations.ConclusionsRapid alternations in all three morphological features assessed have been noticed to be associated with aging in the 45-54 subgroup, suggesting the potential importance of the 5th decade for early preservation method of vascular aging.FundingNational Natural Science Foundation of China.

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“…On the other hand, it should be considered that exposition to tobacco causes damage to DNA, which accelerates senescence in different organs [ 55 ]. In addition to cell cycle arrest, senescent cells secrete an abnormal variety of molecules, including inflammatory cytokines, growth factors, reactive oxygen species (ROS), and extracellular matrix components that modify the cellular microenvironment, which, in turn, causes tissue dysfunction [ 56 ]. The testicular tissue develops senescence in elderly animals [ 57 ]; however, nicotine has not demonstrated to induce this process in the testicle.…”

Section: Discussionmentioning

confidence: 99%

Fetal and Postnatal Nicotine Exposure Modifies Maturation of Gonocytes to Spermatogonia in Mice

Vigueras-Villaseñor

Fuentes-Cano

Chávez-Saldaña

et al. 2020

Analytical Cellular Pathology

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Studies in laboratory animals have shown that male offspring from dams, exposed to nicotine during pregnancy and postnatal periods, show alterations in fertility, although the origin of this is still uncertain. In this study, we examined in a mouse model if the process of gonocyte maturation to spermatogonia was affected in male offspring from dams with nicotine administration during pregnancy and postnatal periods. BALB/C mice, with and without nicotine administrations in pregnancy and postnatal periods, were studied. The animals were euthanized at 3, 7, 10, 16, and 35 days postpartum (dpp). Testicular tissue samples were processed for histological, ultrastructural, and immunohistochemical studies; and testicular lipoperoxidation was determined. It was observed that in the nicotine-exposed animals, there was increased apoptosis and a reduction in the number of gonocytes that matured to spermatogonia. This gonocyte-spermatogonia maturation reduction was associated with a greater immunoreactivity to nicotinic acetylcholine receptors in the germ cells. Lipoperoxidation was similar in both groups until 16 dpp, with significant reduction at 35 dpp. Our findings suggest that nicotine intake during pregnancy and postnatal periods can affect the process of maturation of gonocytes to spermatogonia and the pool of available spermatogonia for spermatogenesis.

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Nicotine in Senescence and Atherosclerosis

Cited by 48 publications

References 234 publications

Nicotine and vascular dysfunction

Nicotine and vascular dysfunction

Morphological alternations of intracerebral arterial during middle age: a community cohort study

Fetal and Postnatal Nicotine Exposure Modifies Maturation of Gonocytes to Spermatogonia in Mice

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