ReviewInternational journal of molecular medicine2026
Lipid droplets in astrocytes: Key organelles for CNS homeostasis and disease (Review).
Review in International journal of molecular medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
6 citing papers in PubMed.
- Convergent Astrocytic Failure in Parkinson's Disease: A System-Level Model of Pathogenesis and Treatment.Molecular neurobiology · 2026Review
- Inter-Organelle Membrane Contact Sites as Physiological Regulatory Hubs in the Brain: From Neurons to Glial Cells.Biomolecules · 2026Review
- Dual-Pathway Astrocyte Failure in Parkinson's Disease: Therapeutic Targeting of Nrf2/TFEB Suppression and cGAS-STING/Ferroptosis Activation.Molecular neurobiology · 2026Review
- HSV-1-Driven Lipid Metabolic Reprogramming and Lipid Droplet Accumulation in Macrophages Impair Antiviral Immunity.Investigative ophthalmology & visual science · 2026Article
- Label-free multiphoton microscopy for intraoperative identification of glioma features and tumor heterogeneity.Frontiers in oncology · 2026Article
- ApoE expression across the CNS: Who, What, Where, When, and How (much)?Molecular neurodegeneration advances · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Astrocytes, the predominant glial cells within the central nervous system, participate in a variety of processes, including metabolic homeostasis, regulation of blood‑brain barrier function, and the integration of neuronal function and structure. Lipids, which are critical components of astrocyte architecture and functionality, play a pivotal role in energy production, membrane fluidity, and the integration of astrocyte‑neuronal structure and function via lipid droplet storage and lipid metabolism. Research indicates that the proper storage of lipid droplets (LDs) in astrocytes is essential for maintaining normal physiological functions of the CNS. Fatty acids released from astrocyte LDs undergo β‑oxidation within mitochondria and are intricately linked to neuronal inflammatory signaling, oxidative stress and mitochondrial energy production. Furthermore, dysregulated lipid metabolism in astrocytes is strongly linked to the onset and progression of neurological disorders. The alteration of lipid metabolic profiles in astrocytes across various microenvironments, along with the identification and screening of critical lipid metabolites, has emerged as a focal point in current research. Nonetheless, the precise mechanisms through which aberrant lipid metabolism in astrocytes influences the onset and progression of neurodegenerative diseases require further elucidation. This article seeks to synthesize recent advancements in the study of LDs‑key organelles responsible for lipid homeostasis in astrocytes‑to elucidate the response characteristics and underlying mechanisms of lipid metabolism in these cells. Furthermore, it aims to investigate the therapeutic potential of inhibiting abnormal lipid secretion and excessive lipid accumulation in astrocytes in the context of neurodegenerative disease progression.
Indexed as
Identifiers
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.