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Illustrated histology of the normal vessel and histological alterations of vascular aging and atherosclerosis. Cross sectional view of the arterial wall. (A) Normal artery. (B) Aged artery. It is characterized by a thickened vessel wall, thickened subendothelial layer, elastin fragments, VSMCs migration and invasion. (C) Atherosclerosis. It is characterized by the accumulation of plaque and the invasion of macrophages and foam cells. 

Illustrated histology of the normal vessel and histological alterations of vascular aging and atherosclerosis. Cross sectional view of the arterial wall. (A) Normal artery. (B) Aged artery. It is characterized by a thickened vessel wall, thickened subendothelial layer, elastin fragments, VSMCs migration and invasion. (C) Atherosclerosis. It is characterized by the accumulation of plaque and the invasion of macrophages and foam cells. 

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Among age-related diseases, cardiovascular and cerebrovascular diseases are major causes of death. Vascular dysfunction is a key characteristic of these diseases wherein age is an independent and essential risk factor. The present work will review morphological alterations of aging vessels in-depth, which includes the discussion of age-related micr...

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... remodeling of vascular structure, resulting in dysfunction of vessels and ultimately, cerebrovascular and cardiovascular diseases. Note that the vascular effects of aging per se should be distinguished from atherosclerosis, which is characterized by a variety of structural changes in the vessel wall including an accumulation of lipids in plaques (Fig. 1). Moreover, aging remodels the vascular wall more diffusely by largely different mechanisms compared to atherosclerosis. Mulvany, et al. [47] and van Varik, et al. [48] hypothesized that vascular remodeling can be classified macroscopically into different types due to the nature of the alterations occuring in the vessel. Vascular ...

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... Aging induces structural modifications in blood vessels, impairs endothelial cell function, and disrupts the integrity of the BBB, a phenomenon confirmed in both humans and aging rodents [74][75][76]. The manifestations of aging-related BBB disruption in humans and animals involve reduced tight junction proteins [77], decreased pericytes [78], and pericyte-induced endothelial gene expression [79]. ...
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Intracerebral hemorrhage (ICH) is the cerebrovascular disease with the highest disability and mortality rates, causing severe damage to the health of patients and imposing a significant socioeconomic burden. Aging stands as a foremost risk factor for ICH, with a significant escalation in ICH incidence within the elderly demographic, highlighting a close association between ICH and aging. In recent years, with the acceleration of the “aging society” trend, exploring the intricate relationship between aging and ICH has become increasingly urgent and worthy of in-depth attention. We have summarized the characteristics of ICH in the elderly, reviewing how aging influences the onset and development of ICH by examining its etiology and the mechanisms of damage via ICH. Additionally, we explored the potential impacts of ICH on accelerated aging, including its effects on cognitive abilities, quality of life, and lifespan. This review aims to reveal the connection between aging and ICH, providing new ideas and insights for future ICH research.
... Aging endothelium or called endothelial cellular senescence. Cells are in a state known as replicative senescence because a cell's ability to procreate is limited 43 . While proliferative senescent cells can sustain an active metabolism for periods then endothelial dysfunction may be exacerbated 44 . ...
... This delayed recovery was confirmed by a lower RMS/M max values for old compared to young during all recovery time point (post-1 min to post-27 min (all P < 0.005). Thus, recovery of quadriceps spinal motoneuron output remained depressed in old subject, potentially due to age-related cortical changes (Oliviero et al. 2006;Rowe et al. 2006;Seidler et al. 2010) and or ii) an altered removal of metabolites due to age-related vasoconstriction and circulatory impairment (Xu et al. 2017), specifically considering that restoration of muscle blood flow and removal of metabolites rapidly attenuates the central effects of group III/IV muscle afferent firing with recovery of VA (Kennedy et al. 2013). This finding aligns with previous research attributing this delayed central fatigue recovery to the prolonged supraspinal fatigue following a sustained high-intensity protocol (Hunter et al. 2008;Yoon et al. 2012). ...
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The aim of the study was to assess the impact of aging on neuromuscular fatigue and recovery. Ten young (23.08 ± 1.43 years) and older (61.19 ± 1.80 years) males performed an intermittent maximal isometric exercise with the knee extensors followed by 27 min of recovery. Maximal voluntary contraction (MVC), total work (W′), voluntary activation (VA), potentiated resting twitch (Ptw), and electromyography (EMG) were recorded and then analyzed. Peripheral and central fatigue following exercise were lower in old compared to young (− 29.99% vs. − 42.68% and − 14.55 vs. − 20.02%; P < 0.05, respectively). Despite old performing 50% less work, RMS/Mmax reduction was similar between old and young (− 26.46% vs. − 29.93%; P > 0.05, respectively). During the recovery period, our results showed that recovery of the MVC was impaired for old (14.93% for old vs. 30.66% for young) and still incomplete until 27 min.VA increased significantly compared to post exercise after 1 min only for young (P = 0.001), potentially affecting the recovery pattern of MVC during the early phase due to their significant correlation (r² = 0.58, P = 0.01). Peripheral fatigue recovery was also lower for old (11.18% vs. 18.72%; P < 0.001), and both groups failed to recover their baseline value (both P < 0.005). The lower peripheral and central fatigue observed in elderly following exercise appears for the first instance as a fatigue resistance. However, the delayed neuromuscular recovery reveals instead a reduced fatigue tolerance reflecting age-related alteration within contractile properties and/or within central nervous system.
... This phenomenon allows the pulse wave to propagate faster, ultimately elevating systolic blood pressure levels [70]. As time progresses, pressure accumulation in the vessel wall induces overproliferation and phenotypic conversion of smooth muscle cells, culminating in the accumulation of extracellular matrix and endothelial dysfunction [71][72][73]. This intricate process is further associated with an imbalance in the release of vasoconstrictors and vasodilators. ...
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Background and Aim The impact of trace elements and heavy metals on human health has attracted widespread attention. However, the correlation between urinary chromium concentrations and blood pressure remains unclear and inadequately reported, and the aim of this study was to investigate the relationship between urinary chromium concentrations and blood pressure in adults in the United States (US). Methods We utilized data from the National Health and Nutrition Examination Survey (NHANES) 2017–2018 for this study. Multivariate logistic regression and multivariate linear regression were used to explore the association of urinary chromium concentrations with hypertension and blood pressure. Additionally, we also performed subgroup analysis and restricted cubic splines (RCS). Results A total of 2958 participants were enrolled in this study. The overall mean systolic blood pressure and diastolic blood pressure were 123.98 ± 0.60, 72.66 ± 0.57 mmHg, respectively. The prevalence of hypertension was found in 41.31% of the whole participants. In the fully adjusted model, we did not observe a correlation between urinary chromium concentrations and the risk of hypertension and systolic blood pressure. However, we found a negative association between urinary chromium concentrations and diastolic blood pressure. In subgroup analysis, we observed a positive association between urinary chromium and the risk of hypertension among participants older than 60 years of age and those who were Non-Hispanic Black. The interaction term highlighted the influence of age and race on this positive association. We also found a negative association of urinary chromium with diastolic blood pressure in male, participants who were current smokers, overweight, and other races, as well as those without alcohol use and anti-hypertensive drug use. However, the interaction term only revealed the influence of alcohol consumption on the negative association. Conclusion Our study suggested that urinary chromium concentrations may show a negative association with diastolic blood pressure and this association was significantly dependent on alcohol consumption. Besides, a positive association between urinary chromium and the risk of hypertension was also found among participants older than 60 years of age and those who were Non-Hispanic Black.
... Consequently, the bridging veins that connect the brain to the skull become more stretched, making them more susceptible to rupture even after minor trauma. This situation leads to intracranial hematomas, including subdural hematomas [17][18][19]. Older patients are more likely to be taking anticoagulant and antiplatelet medications, which increase the risk of bleeding and make hemostasis more difficult. These medications may delay clotting or increase bleeding and hematoma formation after head trauma [16]. ...
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The age-standardized incidence of head trauma in 2016 was 369 per 100,000 people worldwide. The Western Pacific region, including Japan, had the highest incidence. This study aimed to extract ICD-10 code data for intracranial injury (S06) and external causes of morbidity and mortality (V01–Y89), analyze their characteristics and interrelationships, and contribute to these diseases’ prevention, treatment, and prognosis. The number of deaths according to injury type and external cause type of intracranial injury published by the Japanese government was statistically analyzed using JoinPoint, and univariate distribution and multivariate correlation were conducted using JMP Software. From 1999–2021, there was a downward trend in the number of deaths because of intracranial injuries: mortality from intracranial injuries was higher among those aged ≥65 years. Conversely, mortality from intracranial injuries was lower among those aged ≤14 years. Among deaths from intracranial injury, mortality from diffuse brain injury and traumatic subdural hemorrhage was more common. Among deaths from external causes of intracranial injury, mortality from falls, transport accidents, and other unforeseen accidents was more common. Mortality because of intracranial injuries increased significantly during the 2011 Great East Japan Earthquake. For some age groups and sexes, there were significant inverse correlations of mortality with traumatic subdural hemorrhage and traumatic subarachnoid hemorrhage for transport accidents, intentional self-harm and assault, and diffuse brain injury and focal brain injury for falls. We believe that the data presented in this study will be useful for preventing and treating intracranial injuries and for developing administrative measures to reduce intracranial injuries.
... Secondly, device complications were prospectively monitored using rigorous definitions and, in the case of CABSI, blinded outcome assessors. The finding of increasing age being a protective factor against AC failure may be related to the reduced inflammatory response in elderly patients [58], or the effect of aging on vascular endothelium and structural integrity in arteries [59] which warrants further enquiry, Our analysis has some limitations, mainly its exploratory nature and its setting in one country. Due to the low event rates, results should be interpreted with caution, particularly the accidental removal analysis which had fewer patients. ...
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Objectives Arterial catheters (ACs) are critical for haemodynamic monitoring and blood sampling but are prone to complications. We investigated the incidence and risk factors of AC failure. Methods Secondary analysis of a multi-centre randomised controlled trial (ACTRN 12610000505000). Analysis included a subset of adult intensive care unit patients with an AC. The primary outcome was all-cause device failure. Secondary outcomes were catheter associated bloodstream infection (CABSI), suspected CABSI, occlusion, thrombosis, accidental removal, pain, and line fracture. Risk factors associated with AC failure were investigated using Cox proportional hazards and competing-risk models. Results Of 664 patients, 173 (26%) experienced AC failure (incidence rate [IR] 37/1000 catheter days). Suspected CABSI was the most common failure type (11%; IR 15.3/1000 catheter days), followed by occlusion (8%; IR 11.9/1,000 catheter days), and accidental removal (4%; IR 5.5/1000 catheter days). CABSI occurred in 16 (2%) patients. All-cause failure and occlusion were reduced with ultrasound-assisted insertion (failure: adjusted hazard ratio [HR] 0.43, 95% CI 0.25, 0.76; occlusion: sub-HR 0.11, 95% CI 0.03, 0.43). Increased age was associated with less AC failure (60–74 years HR 0.63, 95% CI 0.44 to 0.89; 75 + years HR 0.36, 95% CI 0.20, 0.64; referent 15–59 years). Females experienced more occlusion (adjusted sub-HR 2.53, 95% CI 1.49, 4.29), while patients with diabetes had less (SHR 0.15, 95% CI 0.04, 0.63). Suspected CABSI was associated with an abnormal insertion site appearance (SHR 2.71, 95% CI 1.48, 4.99). Conclusions AC failure is common with ultrasound-guided insertion associated with lower failure rates. Trial registration Australian New Zealand Clinical Trial Registry (ACTRN 12610000505000); date registered: 18 June 2010.
... During the slice positioning of PC-MRI, we carefully placed the imaging plane to be perpendicular to most of the perforating arteries. However, the cerebral perforating arteries tend to become tortuous with age, 35,36 it is possible that the PC-MRI imaging plane may not be perfectly perpendicular to some perforating arteries in elderly adults, leading to a potential underestimation of the mean velocities. Therefore, the velocity results in the present study should be interpreted with caution. ...
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Purpose Directly imaging the function of cerebral perforating arteries could provide valuable insight into the pathology of cerebral small vessel diseases (cSVD). Arterial pulsatility has been identified as a useful biomarker for assessing vascular dysfunction. In this study, we investigate the feasibility and reliability of using dual velocity encoding (VENC) phase‐contrast MRI (PC‐MRI) to measure the pulsatility of cerebral perforating arteries at 7 T. Methods Twenty participants, including 12 young volunteers and 8 elder adults, underwent high‐resolution 2D PC‐MRI scans with VENCs of 20 cm/s and 40 cm/s at 7T. The sensitivity of perforator detection and the reliability of pulsatility measurement of cerebral perforating arteries using dual‐VENC PC‐MRI were evaluated by comparison with the single‐VENC data. The effects of temporal resolution in the PC‐MRI acquisition and aging on the pulsatility measurements were investigated. Results Compared to the single VENCs, dual‐VENC PC‐MRI provided improved sensitivity of perforator detection and more reliable pulsatility measurements. Temporal resolution impacted the pulsatility measurements, as decreasing temporal resolution led to an underestimation of pulsatility. Elderly adults had elevated pulsatility in cerebral perforating arteries compared to young adults, but there was no difference in the number of detected perforators between the two age groups. Conclusion Dual‐VENC PC‐MRI is a reliable imaging method for the assessment of pulsatility of cerebral perforating arteries, which could be useful as a potential imaging biomarker of aging and cSVD.
... Aging: The aging process itself is a significant risk factor for both vascular dysfunction and degenerative diseases [97,98]. As people age, their blood vessels naturally undergo structural and functional changes, becoming less elastic and more susceptible to damage [99]. ...
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Degenerative diseases, encompassing a wide range of conditions affecting various organ systems, pose significant challenges to global healthcare systems. This comprehensive review explores the intricate interplay between the vascular system and degenerative diseases, shedding light on the underlying mechanisms and profound implications for disease progression and management. The pivotal role of the vascular system in maintaining tissue homeostasis is highlighted, as it serves as the conduit for oxygen, nutrients, and immune cells to vital organs and tissues. Due to the vital role of the vascular system in maintaining homeostasis, its dysfunction, characterized by impaired blood flow, endothelial dysfunction, and vascular inflammation, emerges as a common denominator of degenerative diseases across multiple systems. In the nervous system, we explored the influence of vascular factors on neurodegenerative diseases such as Alzheimer’s and Parkinson’s, emphasizing the critical role of cerebral blood flow regulation and the blood–brain barrier. Within the kidney system, the intricate relationship between vascular health and chronic kidney disease is scrutinized, unraveling the mechanisms by which hypertension and other vascular factors contribute to renal dysfunction. Throughout this review, we emphasize the clinical significance of understanding vascular involvement in degenerative diseases and potential therapeutic interventions targeting vascular health, highlighting emerging treatments and prevention strategies. In conclusion, a profound appreciation of the role of the vascular system in degenerative diseases is essential for advancing our understanding of degenerative disease pathogenesis and developing innovative approaches for prevention and treatment. This review provides a comprehensive foundation for researchers, clinicians, and policymakers seeking to address the intricate relationship between vascular health and degenerative diseases in pursuit of improved patient outcomes and enhanced public health.
... Alteration in the mechanical properties of vessel walls as a consequence of age (e.g. vascular stiffening [7]) or pathology (e.g., atherosclerosis) can lead to changes in the degree of pulsatility that is transferred to the microvasculature. Increases in amplitude of the pulsatile blood flow transferred to the cerebral microvasculature have been found to contribute to white matter damage and cognitive decline [8][9][10][11][12]. ...
... Estimations of PI and RI from the long source-detector separation DCS measurements yielded results that fall reasonably within the range of normative values presented previously [37], though deviations are observed. Further investigation of the pulsatile signals across the lifespan as well as in other pathologies could help frame the results presented here in the context of vascular aging as well as vascular pathology [7,49]. From the estimates of pCVR i and pCVC i , we observe changes following the procedure in measurements both ipsilateral and contralateral to the clamping side that are indicative of a greater transfer of blood flow and volume to the cerebral vasculature. ...
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Carotid endarterectomy (CEA) involves removal of plaque in the carotid artery to reduce the risk of stroke and improve cerebral perfusion. This study aimed to investigate the utility of assessing pulsatile blood volume and flow during CEA. Using a combined near-infrared spectroscopy/diffuse correlation spectroscopy instrument, pulsatile hemodynamics were assessed in 12 patients undergoing CEA. Alterations to pulsatile amplitude, pulse transit time, and beat morphology were observed in measurements ipsilateral to the surgical side. The additional information provided through analysis of pulsatile hemodynamic signals has the potential to enable the discovery of non-invasive biomarkers related to cortical perfusion.
... The main pathology of vascular aging is the disorganization and proliferation of the intima-media structure [34]. The pathological structure of the aorta was assessed by H&E staining. ...
... Vascular aging is largely characterized by alterations in their structure and impaired endothelial function [41]. The thickening of the vessel wall in age-related structural remodeling is caused by changes in the intima and media, and an increase in IMT is evident in the aging process [34]. Endothelial dysfunction is significantly influenced by the disparity between vasodilation and contraction. ...
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Vascular aging is an independent risk factor for age-related diseases and a specific type of organic aging. Endothelial progenitor cells (EPCs), a type of bone marrow stem cell, has been linked to vascular aging. The purpose of this study is to investigate if Ginseng-Sanqi-Chuanxiong (GSC) extract, a traditional Chinese medicine, can delay aortic aging in mice by enhancing the performance and aging of EPCs in vivo and to analyze the potential mechanisms through a d-Galactose (D-gal)-induced vascular aging model in mice. Our study revealed that GSC extracts not only enhanced the aortic structure, endothelial function, oxidative stress levels, and aging in mice, but also enhanced the proliferation, migration, adhesion, and secretion of EPCs in vivo, while reducing the expression of p53, p21, and p16. To conclude, GSC can delay vascular senescence by enhancing the function and aging of EPCs, which could be linked to a decrease in p16 and p53/p21 signaling. Consequently, utilizing GSC extracts to enhance the function and senescence of autologous EPCs may present a novel avenue for enhancing autologous stem cells in alleviating senescence.