Academic self-efficacy and online physical education learning engagement: the chain mediating roles of learning motivation and self-control.

Cilia are microtubule-based protrusions that develop on the surface of vertebrate cells during the G0 phase (; ). There are two main types of cilia found in the body: motile cilia and primary cilia. Motile cilia are most frequently assembled as multiple autonomously but synchronously moving organelles originating from a single cell and performing physiological functions by generating local fluid flow. For example, the fluid flow generated by motile cilia in the airway epithelium is essential for inhaled particles. In contrast, primary cilia are generally non-motile sensory organelles, formed as a single structure per cell. Primary cilia harbor various receptors and channels and function as cellular sensors that detect mechanical and fluidic information from the extracellular environment for embryonic development and tissue homeostasis (; ; ). In this review, we will primarily focus on primary cilia and discuss the roles of lipids in their physiological functions, a research paradigm collectively referred to as “lipid ciliology” and defined here as the study of ciliary membrane lipids, their spatiotemporal dynamics, and their disruption in ciliopathies. Morphologically, primary cilia possess four core structures: A basal body i.e, a transformed mother centriole, the transition zone (TZ), the axoneme composed of a microtubule array, and the ciliary membrane (; ; ). Germline mutations and somatic mutations of genes involved in the function and structure of primary cilia cause ciliopathies, a group of rare genetic disorders characterized by clinical symptoms depending on the mutated gene, including polycystic kidney disease, retinopathy, polydactyly, cerebellar hypoplasia, and visceral heterotaxy (; ). Over the past two decades, typical ciliopathies such as Joubert syndrome (JS), Meckel–Gruber syndrome (MKS), Bardet–Biedl syndrome (BBS), and nephronophthisis (NPHP), have been categorized as rare diseases. However, recent findings have suggested that primary cilia play a significant role in the pathophysiology of various common diseases, such as cancers, diabetes, obesity, and atopic dermatitis (; ; ; ). Consequently, ciliology has grown in significance as a field of basic and translational biomedical research. The fundamental etiological mechanism of ciliopathies can be understood as an inability of primary cilia to sense the extracellular environment, resulting in the disruption of downstream signaling pathways. The primary ciliary membrane is enriched in a number of receptors mediating various signaling pathways, such as the Shh, Wnt, and PDGF pathways, as well as ion channels, such as TRP ion channels (; ; ). Thus, the membrane functions as a hub for information exchange between the intracellular and extracellular environments, serving as the point of origin for both extracellular environment detection and intracellular signal transduction. Thus, the primary cilia membrane containing unique proteins and lipids, does not simply serve as a passive structural boundary, but rather functions as a highly compartmentalized hub for receiving extracellular signals. To enable the sensitive detection of extracellular signals, the primary ciliary membrane contains unique protein and lipid components, rather than merely serving as a passive structural boundary essential for the maintenance of signaling fidelity and compartmentalization (; ). Most of the previous cilia-related studies have mainly focused on the protein-based architecture of cilia, such as basal body proteins, TZ proteins, intraflagellar transport (IFT), and signal-transducing receptors. However, recently it has been shown that the lipid composition of the ciliary membrane is also a fundamental determinant of ciliary structure and function (; ). For example, the ciliary membrane displays a highly distinctive phosphoinositide landscape, characterized by elevated levels of phosphatidylinositol 4-phosphate (PI(4)P) and exclusion of phosphatidylinositol 4,5-bisphosphate (PI(4,5)P) () (). The maintenance of the phosphoinositide code in primary cilia relies on inositol polyphosphate 5-phosphatase (INPP5E), which is abundant in the base of the cilium and ciliary axoneme (; ). is one of the genes responsible for JS, the product INPP5E has emerged as a central regulator of ciliary phosphoinositide identity by converting PI(4,5)P to PI(4)P. Loss of INPP5E allows aberrant PI(4,5)P accumulation within the ciliary compartment and disturbs the PI(4)P-enriched, PI(4,5)P signaling (; ). Recently, it was revealed that, in addition to phosphoinositides, sphingolipids, cholesterol, and lysolipids are also ciliary membrane components and are essential for cilia-associated signal transduction (; ; ). Thus, while the earlier review summarized the general roles of lipids in ciliary signaling (), the rapid progress in “lipid ciliology” over the past few years demands an updated synthesis focusing on disease-specific mechanisms. Crucially, significant breakthroughs since 2020 hav