Key result
Lipidomic analysis reveals that platelets shield oxidative lipid metabolism, generating toxic metabolites that escape plasma degradation and deposit at atherosclerotic lesions or thrombi.
Why the study?
To review how lipidomic analysis of intraplatelet compartments and releasates uncovers platelet-lipid interactions, shielded oxidative lipid metabolism, and potential biomarkers or therapeutic targets in atherothrombosis.
This review highlights the role of the platelet lipidome as a 'Trojan horse' that shields toxic lipid metabolites from plasma degradation, contributing to atherothrombosis and offering new biomarker and therapeutic targets.
May implicate platelet lipidome in atherothrombosis; leaves open biomarker and therapeutic validation.
The platelet-lipid chapter in the story of atherothrombosis is an old one, recapitulated and revised in many contexts. For decades several stimulating facets have been added to it, both unraveling and increasing the perplexity of platelet-lipid interplay and its pathophysiological consequences. The recent paradigm shift in our perspective has evolved with lipidomic analysis of the intraplatelet compartment and platelet releasate. These investigations have disclosed that platelets are in constant interaction with circulatory lipids, often reflected in their lipid repertoire. In addition, they offer a shielded intracellular space for oxidative lipid metabolism generating "toxic" metabolites that escape degradation by plasma lipases and antioxidant defense, circulate undetected by conventional plasma lipid profile, and deposited at atherosclerotic lesions or thrombus. Lipidomics divulges this silent invader in platelet vehicles, thereby providing potential biomarkers of pathologic manifestations and therapeutic targets to be exploited, which is surmised in this review.
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Madhumita Chatterjee (2019) conducted a review in Atherothrombosis. Platelet lipidome was evaluated. Lipidomic analysis reveals that platelets shield oxidative lipid metabolism, generating toxic metabolites that escape plasma degradation and deposit at atherosclerotic lesions or thrombi.
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