The Aging Cardiovascular System

Paneni, Francesco; Cañestro, Candela Diaz; Libby, Peter; Lüscher, Thomas F.; Camici, Giovanni G.

doi:10.1016/j.jacc.2017.01.064

Cited by 432 publications

(200 citation statements)

References 156 publications

Supporting

Mentioning

166

Contrasting

Unclassified

Order By: Relevance

“…In vitro experiments show that this metabolic phenotype leads to activation of a pathway involving mitochondrial oxidative stress (mitoOS) and pyruvate kinase M2-mediated STAT3 activation, resulting in increased production of pro-atherogenic IL-6 and IL-1β. Other studies have suggested additional links between mitoOS and human CAD (Paneni et al, 2017), and mitoOS in macrophages increases plaque progression, activates macrophage NF-κB, and promotes the formation of potentially atherogenic neutrophil extracellular traps (NETs) in mouse models of atherosclerosis (Wang et al., 2014; Wang et al, 2017). …”

Section: Energy Metabolism Affects Immune Cell Function In Atherosclementioning

confidence: 99%

Monocyte-Macrophages and T Cells in Atherosclerosis

2017

View full text Add to dashboard Cite

Atherosclerosis is an arterial disease process characterized by the focal subendothelial accumulation of apolipoprotein B-lipoproteins, immune and vascular wall cells, and extracellular matrix. The lipoproteins acquire features of damage-associated molecular patterns and trigger first an innate immune response, dominated by monocyte-macrophages, and then an adaptive immune response. These inflammatory responses often become chronic and non-resolving, leading to arterial damage and thrombosis-induced organ infarction. The innate immune response is regulated at various stages, from hematopoiesis through monocyte changes and macrophage activation. The adaptive immune response is regulated primarily by mechanisms that affect the balance of regulatory vs. effector T cells. Mechanisms related to cellular cholesterol, phenotypic plasticity, metabolism, and aging play key roles in regulating these responses. Herein we review select topics that shed light on these processes and suggest new treatment strategies.

show abstract

Section: Energy Metabolism Affects Immune Cell Function In Atherosclementioning

confidence: 99%

Monocyte-Macrophages and T Cells in Atherosclerosis

2017

View full text Add to dashboard Cite

show abstract

“…Inflammatory conditions are substantially involved in the development of endothelial dysfunction, 53 where IL-1β (interleukin-1β) is one of the key proinflammatory cytokines. Honda et al 54 demonstrated a close relationship between endothelial dysfunction evaluated by flow-mediated dilation and vascular inflammation detected by ( 18 F)-fluorodeoxyglucosepositron emission tomography/computed tomography in subjects with mild cardiovascular risks, both of which were improved after a 6-month antihypertensive treatment.…”

Section: Hallmark Of Disease Inflammationmentioning

confidence: 99%

Endothelial Functions

Godo

Shimokawa

2017

ATVB

379

258

View full text Add to dashboard Cite

e108T he endothelium plays important roles in modulating vascular tone by synthesizing and releasing an array of endothelium-derived relaxing factors, including vasodilator prostaglandins, NO, and endothelium-dependent hyperpolarization (EDH) factors, as well as endothelium-derived contracting factors.1,2 Such redundant mechanisms, like endogenous hyperglycemic hormones, are advantageous for ensuring proper maintenance of vascular tone under pathological conditions, where one of the vasoactive factor-mediated responses is compromised favoring a vasoconstrictor, prothrombotic, and proinflammatory state. Endothelial dysfunction is mainly caused by reduced production or action of endothelium-derived relaxing factors and could be an initial step toward cardiovascular disease.1 Indeed, evaluation of endothelial functions in humans has attracted much attention in the clinical settings because it serves as an excellent surrogate marker of cardiovascular events. For instance, endothelial dysfunction, as evaluated by impaired flow-mediated dilation of the brachial artery or digital reactive hyperemia index in peripheral arterial tonometry, is associated with future cardiovascular events in patients with coronary artery disease, 3-5 and 1-SD decrease in flow-mediated dilation or reactive hyperemia index is associated with doubling of cardiovascular event risk. 6 These observations suggest that endothelial function in peripheral vascular beds could predict future cardiovascular events.In this review, we will sum up the current advances and trends in the research on endothelial functions from bench to bedside with particular focus on recent publications in Arteriosclerosis, Thrombosis, and Vascular Biology. Earlier highlights of the journal on endothelial biology are extensively summarized in some review articles. 7-9 Emerging Modulators of Endothelial Functions Shear StressAs Lüscher and Corti 10 described in an editorial, flow is the signal of life. This physical force is sensed by the endothelium lining internal surface of the whole cardiovascular system to be translated into numerous downstream signaling pathways in a moment to moment manner in response to diverse physiological demands in the body. Indeed, shear stress is one of the important physiological cues that make endothelial cells synthesize and release endothelium-derived relaxing factors to cause relaxation of underlying vascular smooth muscle and vasodilatation. In this context, novel mechanisms of endothelial mechanotransduction in health and disease have been unveiled and summarized in a review series published recently in Arteriosclerosis, Thrombosis, and Vascular Biology. 11,12 Briefly, Zhou et al 12 emphasized the distinct roles of atheroprotective laminar or pulsatile shear stress versus atheroprone oscillatory shear stress or disturbed flow and discussed in detail the underlying molecular mechanisms that are dependent on these patterns of flow. Abe and Berk 11 further reviewed the current knowledge on the dual roles of shear stress with emphasis plac...

show abstract

“…Arterial stiffness results primarily from loss of elastic fibers and an increase in collagen (Fritze et al, 2012). Like AD, cardiovascular disease is another aging‐related disease that brings a great burden for the patients and healthcare systems (Paneni, Diaz Cañestro, Libby, Lüscher, & Camici, 2017). …”

Section: Systems Level Events In Aging and Admentioning

confidence: 99%

Aging and Alzheimer’s disease: Comparison and associations from molecular to system level

et al. 2018

View full text Add to dashboard Cite

Alzheimer's disease is the most prevalent cause of dementia, which is defined by the combined presence of amyloid and tau, but researchers are gradually moving away from the simple assumption of linear causality proposed by the original amyloid hypothesis. Aging is the main risk factor for Alzheimer's disease that cannot be explained by amyloid hypothesis. To evaluate how aging and Alzheimer's disease are intrinsically interwoven with each other, we review and summarize evidence from molecular, cellular, and system level. In particular, we focus on study designs, treatments, or interventions in Alzheimer's disease that could also be insightful in aging and vice versa.

show abstract

The Aging Cardiovascular System

Cited by 432 publications

References 156 publications

Monocyte-Macrophages and T Cells in Atherosclerosis

Monocyte-Macrophages and T Cells in Atherosclerosis

Endothelial Functions

Aging and Alzheimer’s disease: Comparison and associations from molecular to system level

Contact Info

Product

Resources

About