Advances in Cell and Experimental Biology: Cellular Organelle Stress and Homeostasis in Physiology and Diseases

A special issue of Biology (ISSN 2079-7737). This special issue belongs to the section "Cell Biology".

Deadline for manuscript submissions: 30 April 2026 | Viewed by 558

Special Issue Editor


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Guest Editor
Department of Pharmacology, Toxicology, and Therapeutics, The University of Kansas Medical Center, Kansas City, KS 66160, USA
Interests: autophagy; integrated stress response; proteotoxic stress response; organelle homeostasis
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Special Issue Information

Dear Colleagues,

Cellular organelles are specialized compartments within cells that carry out specific functions. For instance, mitochondria are responsible for energy production, the endoplasmic reticulum synthesizes proteins, the Golgi apparatus processes and packages proteins and lipids, cilia sense the environment and move fluids, centrioles are involved in cell division and the DNA damage response, and autophagy lysosomes remove damaged proteins and organelles. Throughout evolution, cells have developed finely tuned mechanisms to adapt to organelle stress and maintain homeostasis. These mechanisms include the unfolded protein response (UPR) and the integrated stress response for the endoplasmic reticulum (ER), the mitochondrial UPR (mtUPR), and mitophagy, which is the autophagic removal of damaged or excess mitochondria. Additionally, there are responses for Golgi stress, DNA damage via centrosomes, and selective autophagy for various cellular organelles, including the endoplasmic reticulum, mitochondria, lipid droplets, Golgi complex, peroxisomes, ribosomes, centrioles, centrosomes, basal bodies, and the cell nucleus. Disruptions in these cellular stress responses and organelle homeostasis can lead to cell dysfunction, resulting in cell death or senescence, and contribute to various diseases such as metabolic disorders, cancer, and neurodegenerative diseases. In this Special Issue, we invite review and original research manuscripts that focus on organelle stress responses in cell physiology and disease. We warmly welcome presenters from the 6th International Conference on Cell and Experimental Biology, as well as all researchers interested in contributing to these exciting topics.

Prof. Dr. Wen-Xing Ding
Guest Editor

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Keywords

  • autophagy
  • integrated stress response
  • proteotoxic stress response
  • organelle homeostasis
  • ubiquitination

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Published Papers (1 paper)

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Research

14 pages, 5375 KB  
Article
Selective Targeting of Senescent FHs74Int Cells by Human Breast Milk Free Fatty Acids
by Tony Tremblay and Lionel Loubaki
Biology 2025, 14(10), 1355; https://doi.org/10.3390/biology14101355 - 3 Oct 2025
Viewed by 366
Abstract
Cellular senescence is a state of irreversible growth arrest characterized by a pro-inflammatory phenotype, playing dual roles in development. In the fetal intestine, the regulation of senescent cells is critical for maintaining tissue homeostasis. Human breast milk (HBM), known for its rich composition [...] Read more.
Cellular senescence is a state of irreversible growth arrest characterized by a pro-inflammatory phenotype, playing dual roles in development. In the fetal intestine, the regulation of senescent cells is critical for maintaining tissue homeostasis. Human breast milk (HBM), known for its rich composition of bioactive molecules, may play a role in modulating senescence, although its effects on senescent intestinal cells remain unexplored. This study investigated whether HBM selectively eliminates senescent cells in the FHs74Int fetal intestinal epithelial cell line. Senescence was assessed via β-galactosidase activity and expression of p16 and p21. The model cell line was treated with HBM, infant formula, and milk fractions, and outcomes included cell recovery, senescence markers, apoptosis, and mitochondrial potential. Total free fatty acids (FFA) were quantified and correlated with senolytic activity. HBM reduced senescent cell recovery without affecting non-senescent cells, correlating with decreased β-galactosidase activity, reduced phospho-p38 and γH2AX expression, mitochondrial depolarization, and caspase activation. Only the lipid fraction retained senolytic activity, which was associated with elevated FFA levels. Incubation of HBM at 37 °C increased FFA content and conferred senolytic activity. These findings are consistent with the idea that HBM exerts selective senolytic effects via FFA, revealing a novel mechanism by which breast milk could contribute to intestinal homeostasis. Full article
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