- Dr. Mingyi Wang, MD, PhD
- Laboratory of Cardiovascular Science, National Institute on Aging, National Institutes of Health, Biomedical Research Center (BRC), Baltimore, MD, USA.
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Special Issue Introduction
The lifespan is sustainably increasing worldwide, leading to aging population. Among age-related preconditioning of tissues that negatively influence life expectancy, cardiovascular aging plays a crucial role. Indeed, the aged cardiovascular tissue exhibits an elevated pro-inflammatory niche, which is characterized by an upregulation of pro-inflammatory molecules oxidative stress and by a down-regulation of the anti-inflammatory counterparts. Within individual cardiovascular cells, pro-inflammatory and oxidative stressor signaling cascades controlling both the expression and function of proteins, mRNA and micro RNA (miRNA) cues are upregulated in cardiovascular cells. With advancing age, on the one hand, an abnormal integration of the proinflammatory and oxidative signaling pathways orchestrating the above-mentioned molecular scenario drives an increase in the necrosis, apoptosis, senescence of the subtype cardiovascular cells such as endothelial cells and cardiomyocytes, and a decrease in the regenerative capacity; on the other hand, it enhances an increase in the proliferation, migration, and invasion of the subtype cardiovascular cells such as vascular smooth muscle cells and fibroblasts. Additionally, age-related phenotypic shifts of cardiovascular cells are accompanied by an increase in the accumulation, deposition, and modification of the extracellular matrix, contributing to a pre-pathological cardiovascular structural and functional restructuring. Interactions among cardiovascular cells, and with the aged microenvironment produce a fertile pro-inflammatory ground, known as age-associated cardiovascular secretory phenotype (AACSP), which drives the onset and progression of cardiovascular diseases such as hypertension, atherosclerosis, heart failure, and stroke via an enhancement of the propensity to a pathologic insult or a decline of the main culprit threshold levels. Importantly, either heart or brain is a part of the specialized vascular system. Indeed, vascular aging is coupled or cross-talked with myocardial and brain aging via proinflammatory signaling. Hence, it contributes to “coupling /decoupling or mismatching conditions” such as cardiovascular failure, impairment of cognition and even dementia such as the Alzheimer’s disease, called “ the age-associated heart-mind syndrome”. In this light, targeting the AACSP may be a new potential therapeutic strategy of the age-associated cardiovascular syndrome.
In this special issue, we aim to supply an updated insight into both physiological and biochemical mechanisms that impact vascular-heart-brain trio cellular and matrix aging in both negative and positive ways. In addition, this special issue would also like to address on the proinflammation and oxidative stressors signaling mechanisms that orchestrate the important cross talk between vascular aging, cardiac and brain related diseases. We believe that this issue will be helpful to the understanding of the underlying pathogenesis of the age-related cardiovascular diseases, as well as to their treatment with both current and new therapeutic approaches.
We invite the potential contributors to contribute original research articles and review articles as well as clinical studies, including case reports, which will stimulate the continuing efforts to understand the etiologies, pathogenesis, diagnosis, treatment and prevention of cardiovascular aging, and the age-associated cardiovascular diseases.
KeywordsEC, VSMC, Fbs, Cardiomyocyte, Non-myocyte, Extracellular matrix, Proinflammation, Cardiovascular aging
Submission Deadline31 Mar 2022