Inflamm-ageing: the role of inflammation in age-dependent cardiovascular disease

Abstract

The ongoing worldwide increase in life expectancy portends a rising prevalence of age-related cardiovascular (CV) diseases in the coming decades that demands a deeper understanding of their molecular mechanisms. Inflammation has recently emerged as an important contributor for CV disease development. Indeed, a state of chronic sterile low-grade inflammation characterizes older organisms (also known as inflamm-ageing) and participates pivotally in the development of frailty, disability, and most chronic degenerative diseases including age-related CV and cerebrovascular afflictions. Due to chronic activation of inflammasomes and to reduced endogenous anti-inflammatory mechanisms, inflamm-ageing contributes to the activation of leucocytes, endothelial, and vascular smooth muscle cells, thus accelerating vascular ageing and atherosclerosis. Furthermore, inflamm-ageing promotes the development of catastrophic athero-thrombotic complications by enhancing platelet reactivity and predisposing to plaque rupture and erosion. Thus, inflamm-ageing and its contributors or molecular mediators might furnish targets for novel therapeutic strategies that could promote healthy ageing and conserve resources for health care systems worldwide. Here, we discuss recent findings in the pathophysiology of inflamm-ageing, the impact of these processes on the development of age-related CV diseases, results from clinical trials targeting its components and the potential implementation of these advances into daily clinical practice.

Characteristics and outcomes of patients hospitalized for COVID-19 and cardiac disease in Northern Italy

“…[2][3][4]14,15,1,17 Inflammatory activation may have a prominent role in the patients with HF and/or CAD, and this may explain their susceptibility to COVID-19 and their poorer clinical course. 18,19,20 Severe hypoxaemia, inflammatory activation, and hypotension may all contribute to myocardial injury during COVID-19, and patients with concomitant CAD or HF may be at higher risk. 21 Recent data show that cardiac injury may occur in 10-30% of unselected patients with COVID-19 and be associated with a severe clinical course and high mortality, independently of a history of cardiovascular disease.…”

“…New pneumonia cases related to the severe acute respiratory syndrome coronavirus (SARS-CoV-2), or coronavirus disease 2019 (COVID- 19), rapidly spread worldwide, establishing critical challenges for the public health and medical communities. The World Health Organization has declared COVID-19 a public health emergency of international concern, with a global estimate of laboratoryconfirmed cases of 1 696 588, and 105 952 deaths as of 12 April 2020.…”

Cellular Signaling Pathways in Medium and Large Vessel Vasculitis

“…Notably, each category of arteries is subject to different disease processes. Atherosclerotic disease, now recognized as a smoldering inflammatory process triggered by subendothelial lipid deposits that spans multiple decades of life, is a major cause of morbidity and mortality (3)(4)(5). In contrast, autoimmune inflammation of arteries is a more aggressive process, complicated by hemorrhage, vessel rupture and vessel occlusion.…”

Redox Imbalances in Ageing and Metabolic Alterations: Implications in Cancer and Cardiac Diseases. An Overview from the Working Group of Cardiotoxicity and Cardioprotection of the Italian Society of Cardiology (SIC)

“…and atherosclerosis) are associated with the increased inflammation mediated by interleukin (IL-) IL-1α, IL-6, IL-8, and increased cellular senescence [14,15], while reactive oxygen species (ROS) mediate the induction of epithelial to mesenchymal transition, inducing tumour cancer metastasis [2,16]. Changes in the epidemiology of cancer and CVDs have also made the co-occurrence of these two diseases more likely, as exemplified by the concomitance of cancer and heart failure (HF).…”

“…This generates an inflammatory state that leads to a vicious circle in which chronic oxidative stress and inflammation feed each other, hence enhancing age-related morbidity and mortality [ 13 ]. Indeed, CV risk factors (i.e., obesity, diabetes, hypertension, and atherosclerosis) are associated with the increased inflammation mediated by interleukin (IL-) IL-1α, IL-6, IL-8, and increased cellular senescence [ 14 , 15 ], while reactive oxygen species (ROS) mediate the induction of epithelial to mesenchymal transition, inducing tumour cancer metastasis [ 2 , 16 ]. Changes in the epidemiology of cancer and CVDs have also made the co-occurrence of these two diseases more likely, as exemplified by the concomitance of cancer and heart failure (HF).…”