Introduction

The “China Cardiovascular Health and Disease Report 2022” shows that the number of patients with cardiovascular diseases (CVDs), including hypertension, coronary heart disease, stroke, and heart failure, has exceeded 330 million, and age-related CVDs rank first in mortality rate among urban and rural residents. Therefore, stress-induced vascular senescence has attracted widespread attention from clinicians and basic research scholars [1]. Vascular aging includes replicative senescence and stress-induced premature senescence. Replicative senescence refers to irreversible cell-cycle arrest caused by telomere shortening during repeated cell division in the absence of external stress, leading to DNA damage and genomic instability. Stress-induced premature senescence refers to irreversible proliferative arrest caused by specific stressors such as persistent DNA damage, oncogene activation, or oxidative stress [2]. Stress-induced premature aging can be reduced or even reversed by improving the stress environment. Thus, this study mainly examined stress-induced vascular senescence.

Stress-induced vascular senescence affects the occurrence and prognosis of CVDs, and OS is a vital factor that induces CVDs [3], 4]. It can also cause vascular dysfunction, manifested as dilation of the vascular lumen, thickening and stiffening of the vascular wall, and reduced vascular compliance and self-repair ability, ultimately leading to vascular remodeling [5]. Intervention in stress-induced vascular senescence is of great significance for delaying human aging and preventing the onset of age-related chronic diseases. Commonly used noninvasive assessment indicators in clinical practice mainly include intimal thickness testing, arterial stiffness measures (including the pulse wave conduction velocity, ankle-brachial index, cardio-malleolar vascular index, reflex wave enhancement index, large artery elasticity index, and small artery elasticity index), and vascular endothelial function tests, including flow-mediated diastolic function to reflect the occurrence and extent of stress-induced vascular senescence [6].

OS is a pathological state in which the production of reactive oxygen species (ROS) exceeds the capacity of cellular antioxidant systems, resulting in ROS accumulation in cells or tissues. Excess ROS damage DNA, proteins, and lipids and can promote apoptosis. Other contributors to stress-induced vascular senescence include inflammation, renin-angiotensin-aldosterone system (RAAS) activation, autophagy dysregulation, telomere/telomerase alterations, mitochondrial dysfunction, and disrupted nitric oxide (NO) signaling [7], 8]. Studies have found that SIRT1 can delay cellular senescence and ameliorate stress-induced vascular senescence through multiple pathways, including antioxidant effects, anti-inflammatory activity, and reduced apoptosis [9].

This review examines stress-induced premature senescence of the vascular wall, with a primary focus on vascular endothelial cells (VECs); it also incorporates evidence from vascular smooth muscle cells (VSMCs) and whole-vessel models to clarify the multicellular contributions to stress-induced vascular senescence. It discusses the key stressors that drive pathological vascular aging, including oxidative stress, chronic inflammation, autophagy dysregulation, telomere attrition, mitochondrial dysfunction, reduced NO bioavailability, and RAAS hyperactivation. It emphasizes mechanistic in vitro and in vivo studies of SIRT1 signaling, rather than clinical trial data, to clarify the underlying molecular pathways. Pathways and regulatory factors were selected based on recurrent hub nodes identified through SIRT1 protein-protein interaction network analysis and based on mechanisms repeatedly confirmed in peer-reviewed literature, ensuring a focused, evidence-based structure.