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Cellular membranes and lipids constitute the essential structural framework of all biological cells, consisting of a complex assembly of phospholipids, cholesterol, sphingolipids, and integral proteins. These components are not merely passive barriers but are active participants in vital processes including signal transduction, vesicle trafficking, and the regulation of membrane-bound enzyme activity (Maxfield & Tabas, 2005). In many pathological states, such as cancer, cardiovascular diseases, and neurodegenerative disorders, the lipid composition and biophysical properties of membranes are significantly altered (Escribá et al., 2008). Therapeutic strategies targeting these structures, often referred to as membrane lipid therapy (MLT), involve the use of molecules that modify membrane fluidity, organization, or lipid signaling to restore homeostasis or selectively destroy pathogens (Barceló-Coblijn et al., 2011). Examples include daptomycin and amphotericin B, which disrupt microbial membranes, and synthetic fatty acids like 2-hydroxyoleic acid that modulate membrane-protein interactions in cancer cells (Taylor & Palmer, 2016). Despite their potential, targeting membranes presents challenges regarding selectivity and systemic toxicity due to the ubiquitous nature of lipid bilayers in the human body (Epand, 2011).
Drugs targeting cellular membranes and lipids typically act through physical disruption of the bilayer, formation of transmembrane pores, alteration of membrane fluidity and thickness, or modulation of lipid-protein interactions to influence signaling cascades (Escribá et al., 2008; Taylor & Palmer, 2016).
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