Alterations in Lysosome Homeostasis in Lipid-Related Disorders: Impact on Metabolic Tissues and Immune Cells
Open accessAbstract
Lipid-related disorders, which primarily affect metabolic tissues, including adipose tissue and the liver are associated with alterations in lysosome homeostasis. Obesity is one of the more prevalent diseases, which results in energy imbalance within metabolic tissues and lysosome dysfunction. Less frequent diseases include Niemann-Pick type C (NPC) and Gaucher diseases, both of which are known as Lysosomal Storage Diseases (LSDs), where lysosomal dysfunction within metabolic tissues remains to be fully characterized. Adipocytes and hepatocytes share common pathways involved in the lysosome-autophagic axis, which are regulated by the function of cathepsins and CD36, an immuno-metabolic receptor and display alterations in lipid diseases, and thereby impacting metabolic functions. In addition to intrinsic defects observed in metabolic tissues, cells of the immune system, such as B cells can infiltrate adipose and liver tissues, during metabolic imbalance favoring inflammation. Moreover, B cells rely on lysosomes to promote the processing and presentation of extracellular antigens and thus could also present lysosome dysfunction, consequently affecting such functions. On the other hand, growing evidence suggests that cells accumulating lipids display defective inter-organelle membrane contact sites (MCSs) established by lysosomes and other compartments, which contribute to metabolic dysfunctions at the cellular level. Overall, in this review we will discuss recent findings addressing common mechanisms that are involved in lysosome dysregulation in adipocytes and hepatocytes during obesity, NPC, and Gaucher diseases. We will discuss whether these mechanisms may modulate the function of B cells and how inter-organelle contacts, emerging as relevant cellular mechanisms in the control of lipid homeostasis, have an impact on these diseases.
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Lipid droplet overload can induce lysosomal defects leading to phagocytosis impairment.
“LD overload could also induce lysosomal defects (49), ultimately leading to phagocytosis impairment.”
From Reducing microglial lipid load enhances β amyloid phagocytosis in an Alzheimer’s disease mouse model (2025) · cites this paper as [49]
The Figure 1 caption says lipid overload induces lysosomal membrane permeabilization in adipose and liver tissues, supporting the lysosomal-defects part of the cited clause. The paper does not specifically identify lipid-droplet overload as the cause. The sentence places the citation before its separate statement about phagocytosis impairment. (LLM, conf=0.78)
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Self-citationWu, Z., Xu, J., Tan, J., Song, Y., Liu, L., Zhang, F., Zhang, Y., Li, X., Chi, Y., & Liu, Y. (2019) · Journal of Cellular and Molecular Medicine · doi:10.1111/jcmm.14232 · Cited by 38 · see citing works
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The exocyst controls lysosome secretion and antigen extraction at the immune synapse of B cells
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Self-citationGenetic and pharmacological evidence implicates cathepsins in Niemann-Pick C cerebellar degeneration
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Flagged first, then by citations
Cited by
Sorted by citations
Reducing microglial lipid load enhances β amyloid phagocytosis in an Alzheimer’s disease mouse model
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“LD overload could also induce lysosomal defects ( 49 ), ultimately leading to phagocytosis impairment.”
Autolysosomal Dysfunction in Obesity-induced Metabolic Inflammation and Related Disorders
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Cholesterol crystals in the pathogenesis of atherosclerosis
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The lysosomal β-glucocerebrosidase strikes mitochondria: implications for Parkinson’s therapeutics
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Impaired lysosomal acidity maintenance in acid lipase-deficient cells leads to defective autophagy
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Endolysosomal vesicles at the center of B cell activation
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Autophagy as a therapeutic linchpin in metabolic diseases and obesity-associated diabetes
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Plasma-targeted proteomic and lipidomic profiling of MASLD, MASH, and hepatitis C virus infection
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- Authors
- Cabrera-Reyes, F., Parra-Ruiz, C., Yuseff, M. I., & Zanlungo, S.
- Affiliations
- Pontificia Universidad Católica de Chile (CL)
- Corresponding author
- Yuseff, María Isabel
- Zanlungo, Silvana
- Venue
- Frontiers in Cell and Developmental Biology
- Publisher
- Frontiers Media SA
- Published
- 2021-12-10
- Volume
- 9
- Pages
- 790568-790568
- ISSN
- 2296-634X (ISSN-L)
- PMC
- PMC8703004
- OpenAlex
- W4200481252
- Cited by
- 24
- References
- 227
- Citations by year
- 2026: 6 · 2025: 6 · 2024: 8 · 2023: 2 · 2022: 2
- FWCI
- 0.46
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Frontiers in Cell and Developmental Biology (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- Agencia Nacional de Investigación y Desarrollo (1180900, 1190334)
- Topics
- Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Lipid metabolism and biosynthesis
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Physiology › Calcium signaling and nucleotide metabolism
- Keywords
- lysosome homeostasis, lysosomal storage disease, Niemann-Pick disease type C, Gaucher disease, obesity, adipocytes, hepatocytes, autophagy, cathepsins, CD36, B cells, antigen processing and presentation, lipid homeostasis, adipose tissue, liver, inflammation
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
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