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Updated: Apr 17, 2026

A Rat Model of Pressure Overload Induced Moderate Remodeling and Systolic Dysfunction as Opposed to Overt Systolic Heart Failure
Published on: April 30, 2020
Age-associated pro-inflammatory remodeling and functional phenotype in the heart and large arteries
1Laboratory of Cardiovascular Science, National Institute on Aging, National Institutes of Health, Biomedical Research Center (BRC), 251 Bayview Blvd, Baltimore, MD 21224, USA.
Insights
Aging causes stress, leading to heart and artery stiffening and high blood pressure. Targeting inflammation may improve this silent cardiovascular syndrome and prevent heart failure.
Area of Science:
- Cardiovascular Science
- Aging Research
- Inflammation Biology
Background:
- The global population is aging, leading to increased age-related cardiovascular stress.
- Aging promotes proinflammatory remodeling in the heart and arteries, involving factors like angiotensin II.
- This results in cardiac and vascular stiffening, hypertension, and impaired ventricular-arterial coupling, often presenting as a silent syndrome.
Purpose of the Study:
- To investigate the role of aging-associated stress and inflammation in cardiovascular remodeling.
- To understand the coupling of proinflammatory signals between the heart and arteries.
- To identify potential therapeutic targets for improving age-related cardiovascular dysfunction.
Main Methods:
- Analysis of age-related structural and functional changes in the heart and vasculature.
- Investigation of the contribution of cardiovascular proinflammatory cells and signaling molecules.
- Examination of the interplay between mechanical and humoral factors in the aging cardiovascular system.
Main Results:
- Aging is characterized by increased proinflammatory remodeling in the heart and arteries.
- This remodeling leads to vascular stiffening, systolic hypertension, and suboptimal ventricular-arterial coupling.
- These changes are driven by cardiovascular proinflammatory cells and linked via common signaling pathways.
Conclusions:
- Targeting proinflammatory signaling molecules presents a promising therapeutic strategy.
- Interventions aimed at reducing inflammation could improve age-associated ventricular-arterial coupling.
- This approach may help prevent cardiovascular events such as heart failure in the aging population.
Abstract:
The aging population is increasing dramatically. Aging-associated stress simultaneously drives proinflammatory remodeling, involving angiotensin II and other factors, in both the heart and large arteries. The structural remodeling and functional changes that occur with aging include cardiac and vascular wall stiffening, systolic hypertension and suboptimal ventricular-arterial coupling, features that are often clinically silent and thus termed a silent syndrome. These age-related effects are the result of responses initiated by cardiovascular proinflammatory cells. Local proinflammatory signals are coupled between the heart and arteries due to common mechanical and humoral messengers within a closed circulating system. Thus, targeting proinflammatory signaling molecules would be a promising approach to improve age-associated suboptimal ventricular-arterial coupling, a major predisposing factor for the pathogenesis of clinical cardiovascular events such as heart failure.
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