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Cells
Special Issues
Lipid Homeostasis: Mechanisms, Regulation, and Implications for Health and Disease
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Lipid Homeostasis: Mechanisms, Regulation, and Implications for Health and Disease

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Biophysics".

Deadline for manuscript submissions: 25 March 2026 | Viewed by 1911

Special Issue Editors

Prof. Dr. Roger Schneiter

E-Mail Website
Guest Editor
Department of Biology, University of Fribourg, Chemin du Musée 10, CH-1700 Fribourg, Switzerland
Interests: membrane homeostasis; lipid droplet biogenesis; lipid transport; sterol export; CAP proteins; fatty acid transport
Special Issues, Collections and Topics in MDPI journals
Dr. Museer Ahmad Lone

E-Mail Website
Guest Editor
Institute of Clinical Chemistry, University Hospital of Zurich, Zurich, Switzerland
Interests: lipid homeostasis in mammals; lipidomics; sphingolipids; rare genetic disorders

Special Issue Information

Dear Colleagues,

Lipid homeostasis is fundamental to cellular function, energy storage, and membrane dynamics, impacting a wide range of physiological processes and disease states. This Special Issue seeks contributions that explore recent advances in lipid metabolism, regulatory pathways, and lipid-related cellular functions. We welcome studies on lipid synthesis and degradation, lipid transport and signaling, the role of lipids in metabolic diseases, and mechanisms underlying lipid balance in response to environmental and genetic factors. Submissions may include original research, reviews, and perspectives on the molecular regulation of lipid homeostasis, lipid–protein interactions, lipidomics, and emerging therapeutic approaches targeting lipid imbalances in metabolic disorders. By bringing together diverse insights, this Issue aims to advance our understanding of lipid homeostasis and inspire new strategies for disease prevention and treatment.

Prof. Dr. Roger Schneiter
Dr. Museer Ahmad Lone
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • lipid metabolism
  • lipid synthesis and degradation
  • triglyceride storage
  • fatty acid oxidation
  • cholesterol homeostasis
  • adipogenesis
  • lipid droplets
  • lipid signaling pathways
  • lipid transport proteins
  • phospholipid balance
  • sphingolipid metabolism
  • sterol regulatory element-binding proteins (SREBPs)
  • AMP-activated protein kinase (AMPK)
  • peroxisome proliferator-activated receptors (PPARs)
  • insulin signaling and lipid storage
  • endoplasmic reticulum stress and lipids
  • lipoprotein metabolism
  • non-alcoholic fatty liver disease (NAFLD)
  • lipidomics
  • autophagy and lipid recycling
  • lysosomal lipid degradation
  • lipid-binding proteins
  • oxidized lipids
  • lipid imbalance and disease
  • energy homeostasis and lipid storage
  • lipid transport vesicles
  • membrane lipid composition
  • lipid peroxidation
  • lipid-related genetic disorders, nutrient sensing and lipid regulation

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Further information on MDPI's Special Issue policies can be found here.

Published Papers (2 papers)

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Research

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15 pages, 2661 KB  
Article
miR-451 Is a Driver of Lipotoxic Injury in Patients with Diabetic Cardiomyopathy
by Sarah Costantino, Shafeeq A. Mohammed, Federico Ranocchi, Francesco Zito, Valentina Delfine, Nazha Hamdani, Maria Cristina Vinci, Giovanni Melina and Francesco Paneni
Cells 2025, 14(17), 1401; https://doi.org/10.3390/cells14171401 - 8 Sep 2025
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Abstract
MicroRNA 451 (miR-451) is emerging as a pivotal mediator of cardiac damage in experimental models of diabetic cardiomyopathy. Whether miR-451 plays a detrimental role in the human diabetic myocardium is unknown. The present study investigates miR-451’s role in patients with type 2 diabetes [...] Read more.
MicroRNA 451 (miR-451) is emerging as a pivotal mediator of cardiac damage in experimental models of diabetic cardiomyopathy. Whether miR-451 plays a detrimental role in the human diabetic myocardium is unknown. The present study investigates miR-451’s role in patients with type 2 diabetes (T2D). We show that miR-451 is upregulated in myocardial specimens from T2D patients compared to controls without diabetes and correlates with cardiometabolic parameters, the myocardial triglyceride content and cardiac expression of lipotoxic genes as well as echocardiographic indices of left ventricular dysfunction. Calcium-binding protein 39 (Cab39)—a known target of miR-451 in mouse hearts—was downregulated in T2D patients vs. controls, and its expression negatively correlated with that of miR-451. In cultured human cardiomyocytes (CMs), Ago2 immunoprecipitation confirmed Cab39 to be a direct target of miR-451. Treatment with a high amount of glucose (25mM) and palmitic acid (PA) mimicked miR-451 upregulation and Cab39 downregulation in human CMs. These changes were associated with increased TGs and markers of lipotoxic injury, such as elevated oxidative stress levels, mitochondrial dysfunction and apoptosis. Targeting miR-451 led to restoration of Cab39 levels while rescuing diabetes-induced lipotoxic injury and metabolic dysfunction. By contrast, miR-451 overexpression recapitulated features of lipotoxic damage. Our findings indicate miR-451 to be a potential target for the prevention of myocardial lipotoxic injury in diabetes. Full article
(This article belongs to the Special Issue Lipid Homeostasis: Mechanisms, Regulation, and Implications for Health and Disease)
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Review

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31 pages, 1647 KB  
Review
PCSK9 Regulation of Lipid Metabolism in the Nervous System: Implications for Schwann Cell Function and Peripheral Neuropathy
by Agnieszka Nowacka, Maciej Śniegocki and Ewa A. Ziółkowska
Cells 2025, 14(18), 1479; https://doi.org/10.3390/cells14181479 - 22 Sep 2025
Viewed by 349
Abstract
Neural function relies on tightly regulated lipid metabolism to sustain membrane integrity, synaptic signaling, and energy production. Myelinating glia, particularly Schwann cells, require continuous lipid flux to build and maintain myelin, rendering them vulnerable to imbalances between lipid entry and oxidative capacity. Proprotein [...] Read more.
Neural function relies on tightly regulated lipid metabolism to sustain membrane integrity, synaptic signaling, and energy production. Myelinating glia, particularly Schwann cells, require continuous lipid flux to build and maintain myelin, rendering them vulnerable to imbalances between lipid entry and oxidative capacity. Proprotein convertase subtilisin/kexin type 9 (PCSK9), widely studied in hepatic cholesterol regulation, has emerging roles in the nervous system. In the central nervous system (CNS), local PCSK9 expression influences low-density lipoprotein receptor (LDLR) family abundance, neuronal survival pathways, and neuroinflammatory tone, although circulating PCSK9 has limited parenchymal access due to the blood–brain barrier (BBB). In the peripheral nervous system (PNS), recent evidence highlights a PCSK9–CD36 axis in Schwann cells; genetic Pcsk9 loss elevates CD36, increases fatty-acid influx, promotes lipid droplet expansion and acylcarnitine accumulation, and triggers mitochondrial stress that manifests as hypomyelination, C-fiber pathology, and selective small-fiber neuropathy. These findings suggest that PCSK9 normally restrains CD36-dependent transport to align lipid supply with metabolic demand. Clinically, PCSK9 inhibitors have demonstrated cardiovascular benefit without major neurocognitive signals, yet small-fiber outcomes have not been systematically assessed. This review integrates current evidence on PCSK9 biology across neural compartments, highlights mechanistic links to Schwann cell lipid handling, and outlines research priorities to resolve neural safety and therapeutic potential in lipid-driven neuropathies. Full article
(This article belongs to the Special Issue Lipid Homeostasis: Mechanisms, Regulation, and Implications for Health and Disease)
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