Extracellular vesicles (EVs) are small vesicles released by the majority of cells in response to cell activation or death stimuli. They are grouped as small EVs or exosomes, large EVs such as microvesicles (MVs) and apoptotic bodies, resulting from distinct mechanisms of generation. EVs are released into the extracellular space, in most human biological fluids and tissues, including atherosclerotic plaques. They transport complex cargo of bioactive molecules, including proteins, lipids and genetic material and are therefore involved in pathophysiological pathways of cell-cell communication. Indeed, EVs are involved in several processes such as inflammation, coagulation, vascular dysfunction, angiogenesis and senescence, contributing to the initiation and progression of atherothrombotic diseases. Consequently, they behave as a determinant of atherosclerotic plaque vulnerability leading to major cardiovascular disorders. Over the last decade, the field of EVs research has grown, highlighting their involvement in atherosclerosis. However, limitations in both detection methodologies and standardisation have hindered implementation of EVs in the clinical settings. This review summarizes the effect of EVs in atherosclerosis development, progression and severity, with specific attention devoted to their ambivalent roles in senescence and hemostasis. This review will also highlight the role of MVs as multifaceted messengers, able to promote or to attenuate atherosclerosis progression. Finally, we will discuss the main technical challenges and prerequisites of standardization for driving EVs to the clinics and delineate their relevance as emergent biomarkers and innovative therapeutic approaches in atherosclerosis.

The fundamental role of cell adhesion molecules in mediating various biological processes as angiogenesis has been well-documented. CD146, an adhesion molecule of the immunoglobulin superfamily, and its soluble form, constitute major players in both physiological and pathological angiogenesis. A growing body of evidence shows soluble CD146 to be significantly elevated in the serum or interstitial fluid of patients with pathologies related to deregulated angiogenesis, as autoimmune diseases, obstetric and ocular pathologies, and cancers. To block the undesirable effects of this molecule, therapeutic antibodies have been developed. Herein, we review the multifaceted functions of CD146 in physiological and pathological angiogenesis and summarize the interest of using monoclonal antibodies for therapeutic purposes.

Levodopa (L‐dopa) remains the basis of pharmacological treatment of Parkinson's disease (PD). However, L‐dopa therapy is associated with the development of complications and presents major challenges in the long‐term treatment. Thus, other medications may be suggested to delay and/or reduce the doses of L‐dopa in order to prevent complications. The interpretation of treatment evolution reported in clinical trials on PD may be tricky, especially due to some variability in medications and dose regimens. Some authors have suggested a conversion factor to generate a total L‐dopa equivalent daily dose (LEDD), calculated as a sum of each parkinsonian medication. Therefore, LEDD provides an artificial summary of the total daily medication a patient is receiving, and to date, there is no report focusing on the clinical interpretation of this parameter. Thus, based on a 3‐year, multi‐center retrospective study assessing the impact of second‐line therapy initiation on LEDD in PD patients, the aim of our article was to discuss LEDD as a quantitative outcome to estimate the impact of second‐line therapies on medication regimens; and in the second part of the discussion, to provide a narrative review of the clinical outcomes associated with LEDD in the literature.