Abdominal aortic aneurysm (AAA) is a life-threatening disease associated with high morbidity, and high mortality in the event of aortic rupture. Major advances in open surgical and endovascular repair of AAA have been achieved during the past 2 decades. However, drug-based therapies are still lacking, highlighting a real need for better understanding of the molecular and cellular mechanisms involved in AAA formation and progression. The main pathological features of AAA include extracellular matrix remodelling associated with degeneration and loss of vascular smooth muscle cells and accumulation and activation of inflammatory cells. The inflammatory process has a crucial role in AAA and substantially influences many determinants of aortic wall remodelling. In this Review, we focus specifically on the involvement of monocytes and macrophages, summarizing current knowledge on the roles, origin, and functions of these cells in AAA development and its complications. Furthermore, we show and propose that distinct monocyte and macrophage subsets have critical and differential roles in initiation, progression, and healing of the aneurysmal process. On the basis of experimental and clinical studies, we review potential translational applications to detect, assess, and image macrophage subsets in AAA, and discuss the relevance of these applications for clinical practice.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1038/nrcardio.2017.52 | DOI Listing |
J Exp Clin Cancer Res
March 2025
Peter MacCallum Cancer Centre, Melbourne, VIC, 3000, Australia.
In the last two decades, novel and promising cell-based therapies have populated the treatment landscape for haematological tumors. However, commonly exploited T and NK cell-based therapies show limited applicability to solid tumors. This is mainly given by the impaired tumor trafficking capability and limited effector activity of these cells within a highly immunosuppressive tumor microenvironment.
View Article and Find Full Text PDFToxicology
March 2025
Division of Pharmacology and Toxicology, College of Pharmacy, University of Texas at Austin, Austin, TX, 78712, USA.
Mono-(2-ethylhexyl) phthalate (MEHP) is a metabolite of the diester parent compound Di(2-ethylhexyl) phthalate (DEHP), a widespread environmental toxicant known for its harmful effects on Sertoli cells and the subsequent loss of germ cells through apoptosis in postnatal animals. Peritubular myoid cells (PTMCs) produce various signaling factors, including the chemokine monocyte chemotactic protein 1 (MCP-1); however, the MEHP exposure-induced BTB disruption followed by MCP-1 secretion by PTMCs, the recruitment, and activation of macrophages as well as molecular mechanisms that initiate the secretion in the testis has yet to be closely examined. In this study, we demonstrate for the first time that PTMCs generate MCP-1 via the interleukin-1 signaling pathway upon MEHP exposure.
View Article and Find Full Text PDFInt J Cardiol
March 2025
Laboratory for Experimental Cardiology, Department of Cardiology, University Medical Center Utrecht, Utrecht, the Netherlands. Electronic address:
Background: Inflammatory conditions such as obesity and diabetes are linked to intermediate/non-classical monocyte activation, contributing to left ventricular diastolic dysfunction (LVDD) and heart failure with preserved ejection fraction (HFpEF).
Objective: To investigate whether circulating monocyte subtypes and their activity are associated with the presence LVDD and HFpEF.
Methods: We analyzed peripheral blood mononuclear cells (PBMCs) from 73 patients with or without LVDD/HFpEF.
J Transl Med
March 2025
Department of Clinical-Surgical, Diagnostic and Pediatric Sciences, Università degli Studi di Pavia, Pavia, Italy.
Biol Direct
March 2025
Department of Pediatric Cardiology, Cheeloo Colledge of Medicine, Shandong Provincial Hospital, Shandong University, Jinan, Shandong, China.
Background: Viral myocarditis (VMC) is an inflammatory myocardial condition triggered by viral infections which involves pathogenic-related damage and immune-mediated damage. However, the precise immunopathogenic mechanisms underlying VMC remain elusive.
Methods: We performed single-cell RNA sequencing on mouse hearts during the acute phase of CVB3-induced VMC.
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!