Non-coding RNAs (ncRNAs) represent a broad family of molecules that regulate gene expression, including microRNAs, long non-coding RNAs and circular RNAs, amongst others. Dysregulated expression of ncRNAs alters gene expression, which is implicated in the pathogenesis of several malignancies and inflammatory diseases. Gastric cancer is the fifth most frequently diagnosed cancer and the fourth most common cause of cancer-related death. Studies have found that altered expression of ncRNAs may contribute to tumourigenesis through regulating proliferation, apoptosis, drug resistance and metastasis. This review describes the potential use of ncRNAs as diagnostic and prognostic biomarkers. Moreover, we discuss the involvement of ncRNAs in the pathogenesis of gastric cancer, including their interactions with the members of major signalling pathways.

Atherosclerosis is a condition that is associated with lipid accumulation in the arterial intima. Consequently, the enlarging lesion, which is also known as an atherosclerotic plaque, may close the blood vessel lumen, thus leading to organ ischaemia. Furthermore, the plaque may rupture and initiate the formation of a thrombus, which can cause acute ischaemia. Atherosclerosis is a background pathological condition that can eventually lead to major cardiovascular diseases such as acute coronary syndrome or ischaemic stroke. The disorder is associated with an altered profile of alarmins, stress response molecules that are secreted due to cell injury or death and that induce inflammatory responses. High-mobility group box 1 (HMGB1), S100 proteins, interleukin-33, and heat shock proteins (HSPs) also affect the behaviour of endothelial cells and vascular smooth muscle cells (VSMCs). Thus, alarmins control the inflammatory responses of endothelial cells and proliferation of VSMCs, two important processes implicated in the pathogenesis of atherosclerosis. In this review, we will discuss the role of alarmins in the pathophysiology of atherosclerosis and myocardial infarction.

Hypertrophic cardiomyopathy (HCM) is the most prevalent hereditary cardiovascular disorder, characterised by left ventricular hypertrophy and cardiac fibrosis. Cardiac fibroblasts, transformed into myofibroblasts, play a crucial role in the development of fibrosis. However, interactions between fibroblasts, cardiomyocytes, and immune cells are considered major mechanisms driving fibrosis progression. While the disease has a strong genetic background, its pathogenetic mechanisms remain complex and not fully understood. Several signalling pathways are implicated in fibrosis development. Among these, transforming growth factor-beta and angiotensin II are frequently studied in the context of cardiac fibrosis. In this review, we summarise the most current evidence on the involvement of signalling pathways in the pathogenesis of HCM. Additionally, we discuss the potential role of monitoring pro-fibrotic molecules in predicting clinical outcomes in patients with HCM.

Hepatitis C virus (HCV) is a hepatotropic virus that can be transmitted through unsafe medical procedures, such as injections, transfusions, and dental treatment. The infection may be self-limiting or manifest as a chronic form that induces liver fibrosis, cirrhosis, or progression into hepatocellular carcinoma (HCC). Epigenetic mechanisms are major regulators of gene expression. These mechanisms involve DNA methylation, histone modifications, and the activity of non-coding RNAs, which can enhance or suppress gene expression. Abnormal activity or the dysregulated expression of epigenetic molecules plays an important role in the pathogenesis of various pathological disorders, including inflammatory diseases and malignancies. In this review, we summarise the current evidence on epigenetic mechanisms involved in HCV infection and progression to HCC.

Subclavian artery pseudoaneurysms are rare but potentially life-threatening vascular injuries frequently associated with trauma such as clavicle fractures. In this paper we describe the case of a 49-year-old male who developed a post-traumatic pseudoaneurysm of the subclavian artery after a bicycle accident. The diagnosis was delayed due to non-specific symptoms and an initially missed aneurysm on computed tomography imaging. Persistent pain, swelling, and erythema in the subclavian region prompted further detailed diagnostics, which ultimately revealed the pseudoaneurysm. The patient was successfully treated with endovascular stent–graft implantation. We screened the PubMed database to identify similar cases managed exclusively through endovascular intervention. Reports of iatrogenic pseudoaneurysms and those treated with open surgery were excluded. Variables such as time to diagnosis, clinical presentation, features of pseudoaneurysms, and complications were analyzed to highlight the role of endovascular techniques as a minimally invasive and effective treatment option. These cases pose both a diagnostic and a therapeutic challenge, as early recognition of symptoms is crucial to prevent serious complications including thrombosis, neurological deficits, and even limb loss.

Median Arcuate Ligament Syndrome, also known as Dunbar’s syndrome, is a rare condition caused by stenosis of the celiac artery (CAS) through the fibrous arch connecting the diaphragmatic branches. It manifests as postprandial abdominal pain, nausea, vomiting, weight loss and increased epigastric tenderness. The condition most commonly affects young females without coexisting vascular comorbidities. Diagnosis is difficult due to the non-specific symptoms, often overlapping with other gastrointestinal diseases. Standard investigations include duplex ultrasound, computed tomography angiography (CTA) and contrast-enhanced magnetic resonance imaging (CE-MRA). Treatment mainly consists of surgical release of the arch ligament, which can be performed by open, laparoscopic or robotic methods. Surgery is often supported by celiac truncal stenting for residual stenosis, which significantly improves vascular flow. Alternative approaches include visceral plexus blocks and novel hybrid techniques, such as a combination of ligament release and endovascular treatment of the celiac trunk. In severe cases, vascular by-passes are recommended. The aim of this paper is to discuss the clinical manifestations, diagnostic possibilities, therapeutic options and directions for further research on MALS from the perspective of a vascular surgeon. It emphasizes the need for a multidisciplinary approach, including collaboration between the surgeon, radiologist, gastroenterologist and psychologist, which enables comprehensive disease management and improved quality of life for patients. In addition, the need for further development of diagnostic and therapeutic methods for early diagnosis and effective treatment was pointed out.