Abdominal aortic aneurysm (AAA) is a type of cardiovascular disease. Sudden aortic rupture and subsequent bleeding are the main causes of mortality due to AAA. N6‑methyladenosine (m6A) methylation, the most common epitranscriptomic modification in eukaryotic mRNAs, has a key role in the regulation of gene expression. m6A methylation markedly influences the development and progression of AAA. The present review highlights the mechanism of m6A methylation in AAA, including current research progress and future prospects. From a mechanistic perspective, m6A methylation exerts its influence on AAA‑related genes by modulating the post‑transcriptional levels of RNA, thereby impacting the pathological process of AAA. In terms of clinical applications, the mechanisms by which m6A methylation regulators influence their development and progression in AAA involve multiple target genes and signaling pathways. These regulatory factors affect inflammatory immunomodulation, cell proliferation, apoptosis and endogenous processes by modulating the m6A modification status of target genes and the activity of immune‑related signaling pathways. Therefore, for the prevention and treatment of AAA, current therapeutic strategies should comprehensively consider the interactions and synergistic regulation among m6A methylation regulators to reveal the integrated effects of the entire regulatory network in AAA development. Consequently, a more comprehensive understanding of the precise mechanisms of m6A methylation in AAA should be attained, which will support the development of innovative therapeutic strategies aimed at m6A methylation and establish a basis for the early diagnosis and treatment of AAA.

The pathobiology of aortic disease is linked to aortic region: atherosclerosis for abdominal aorta, primary medial degeneration or aortitis for ascending thoracic aorta, and all causes for descending thoracic aorta and thoracoabdominal lesions. The pathogenesis of aortic dissection involves damage of the outer media from impaired perfusion from dysfunctional vasa vasorum, formation of discrete foci of disrupted vascular smooth muscle cell-elastic fiber extension-contractile units, and imbalance of radial sheer stress across the aortic wall, thereby creating an intimal tear and linear dissection. Thoracic aortic aneurysms develop from the chronic progression of medial degeneration coupled with the weakening of the remodeled adventitia, allowing for aortic dilatation. Precipitating factors include hypertension and mutations of genes regulating the vascular smooth muscle cell-elastic fiber extension-contractile units. Criteria are presented for distinguishing genetic from acquired causes of thoracic aortic aneurysms and dissections, with important implications for therapeutic and surgical decisions in the care of these patients.

An aneurysm is defined as a dilation of the arterial wall with a diameter exceeding 1.5 times the normal diameter of the vessel concerned. Aortic aneurysms (AAs) can develop at any level but are mostly found at the abdominal and infrarenal levels and extend to the iliac arteries. AAs are usually asymptomatic and are most often discovered incidentally during various imaging investigations for other conditions. Rupture of an AA is usually dramatic, being one of the causes of sudden cardiac death. Surgical treatment and, more recently, endovascular treatment are the only effective methods of AA repair. In this study, we screened for the diagnosis of AAs in patients with stable exertional angina who had indications for coronary angiography. The study was carried out in the period 2021-2023 in the Institute of Cardiovascular Diseases Timişoara, Romania. Of the 2458 patients with exertional angina who required coronary angiography, a number of 1844 (75%) patients had at least one stenotic atheromatous plaque, and of these 312 patients had AAs, of which 173 at the level of the abdominal aorta.