Fighting time in our blood vessels: how science aims to preserve vascular health
image: Vascular aging is a complex pathophysiological process propelled by endothelial dysfunction, oxidative stress, chronic inflammation, cellular senescence, endothelial stiffening, and vascular smooth muscle cell (VSMC) alterations. These interconnected mechanisms drive a self-reinforcing cycle that progressively compromises vascular integrity, exacerbates endothelial dysfunction, and accelerates aging. Ultimately, this cycle promotes vascular stiffness and maladaptive remodeling—hallmarks of aged vessels—and significantly increases susceptibility to cardiovascular diseases.
Credit: Aging Research, Tsinghua University Press
As life expectancy rises worldwide, the wear and tear on our blood vessels becomes a pressing health challenge. Aging arteries are more prone to stiffness, calcification, and inflammation, setting the stage for heart disease, strokes, kidney failure, and cognitive decline. This deterioration doesn’t just threaten longevity—it erodes quality of life, limiting mobility and organ performance. Detecting vascular aging early is difficult, and current treatments often address symptoms rather than root causes. Due to these challenges, there is an urgent need to uncover the cellular and molecular drivers of vascular aging and develop precise, targeted strategies to preserve vascular function across the lifespan.
CHICAGO, March 27, 2025 — Scientists at the University of Illinois Chicago have pieced together a detailed picture of what happens to our blood vessels as we age, and how to fight back. In a comprehensive review (DOI: 10.26599/AGR.2025.9340039) published in Aging Research, the team connects the dots between microscopic changes in endothelial cells, the build-up of oxidative damage, and the stiffening of artery walls. They also evaluate emerging diagnostics and therapies—spanning lifestyle habits, targeted drugs, and regenerative medicine—that could transform vascular aging from an unavoidable fate into a preventable condition.
The review identifies six interlocking processes at the heart of vascular aging: endothelial dysfunction, oxidative stress, chronic inflammation, extracellular matrix remodeling, vascular smooth muscle cell changes, and telomere shortening. Central to this decline are molecular players like Caveolin-1, which regulates nitric oxide—a molecule essential for vessel flexibility—and Nucleoporin-93, which safeguards cellular transport and prevents inflammation. When these systems falter, blood vessels lose their ability to relax, repair, and resist damage. Biomarkers such as reduced nitric oxide levels, high von Willebrand factor, elevated endothelin-1, and shortened telomeres provide early warning signs. The authors emphasize that oxidative stress and inflammation feed off each other, accelerating arterial stiffening, while imbalances in structural proteins like collagen and elastin further erode vessel resilience. Potential countermeasures range from aerobic exercise and Mediterranean diets to targeted antioxidants like mitoTEMPO, which neutralizes harmful mitochondrial molecules without disrupting essential cell signals. Looking further ahead, therapies such as senolytic drugs, stem cell transplants, epigenetic modulators, and CRISPR-based gene editing could one day repair or rejuvenate aging vessels—if challenges in safety and delivery can be overcome.
“Vascular aging is far from a fixed destiny,” said Jiwang Chen, senior author of the review. “It is a biological process we can influence—sometimes profoundly—through the right combination of lifestyle choices and precision medical interventions. By targeting the cellular pathways that drive vessel decline, we have the potential not only to reduce the burden of heart and brain disease, but to help people stay active, independent, and healthy well into older age. Our review highlights the science guiding us toward that future.”
The insights from this work could reshape both prevention and treatment. Clinicians may one day use vascular biomarkers to predict disease risk years before symptoms appear, tailoring interventions to each patient’s biology. Public health programs could integrate dietary guidance, physical activity, and smoking cessation into community-based vascular health initiatives. Meanwhile, research targeting molecules like Caveolin-1, NUP93, and telomerase could lead to transformative therapies for age-related diseases. The long-term vision is bold: to delay vascular aging itself, thereby reducing the cascade of health problems it triggers and extending not only how long we live, but how well we live those years.
About Aging Research
Aging Research is an Open Access publication addressing the biology and medicine issues of aging and aging-related diseases. Aging Research publishes original research results that are of unusual significance or broad conceptual or technical advances in all areas of aging, longevity and aging related health issues. The journal focuses on the following research: to explore the process, mechanism, biomarkers, anti-aging strategies or drugs at the population, individual, system, organ, tissue, cell and subcellular levels; to study the epidemiological characteristics, pathogenesis, pathophysiological processes, diagnostic criteria, clinical experiments and translational research of age-related diseases.