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Lysosomes are digestive organelles that are crucial for nutrient sensing and metabolism. Lysosome impairment is linked to a broad spectrum of metabolic disorders, underscoring their importance to human health. Thus, lysosomes are an attractive target for metabolic disease therapies.

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Assessing the impact of TiO nanomaterials on intestinal cells: New evidence for epithelial translocation and potential pro-inflammatory effects.

Toxicology

January 2025

National Institute of Health Doutor Ricardo Jorge, I.P (INSA), Department of Human Genetics, Lisbon, Portugal; bCentre for Toxicogenomics and Human Health (ToxOmics), NOVA Medical School, Universidade NOVA de Lisboa, Lisbon, Portugal. Electronic address:

Understanding the potential impact of nanomaterials (NMs) on human health requires further investigation into the organ-specific nano-bio interplay at the cellular and molecular levels. We showed increased chromosomal damage in intestinal cells exposed to some of in vitro digested Titanium dioxide (TiO) NMs. The present study aimed to explore possible mechanisms linked to the uptake, epithelial barrier integrity, cellular trafficking, as well as activation of pro-inflammatory pathways, after exposure to three TiO-NMs (NM-102, NM-103, and NM-105).

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Vacuolization of hematopoietic precursors cells is a common future of several otherwise non-related clinical settings such as VEXAS, Chediak-Higashi syndrome and Danon disease. Although these disorders have a priori nothing to do with one other from a clinical point of view, all share abnormal vacuolization in different cell types including cells of the erythroid/myeloid lineage that is likely the consequence of moderate to drastic dysfunctions in the ubiquitin proteasome system and/or the endo-lysosomal pathway. Indeed, the genes affected in these three diseases UBA1, LYST or LAMP2 are known to be direct or indirect regulators of lysosome trafficking and function and/or of different modes of autophagy.

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Pathological cardiac remodeling is a maladaptive response that leads to changes in the size, structure, and function of the heart. These changes occur due to an acute or chronic stress on the heart and involve a complex interplay of hemodynamic, neurohormonal and molecular factors. As a critical regulator of cell growth, protein synthesis and autophagy mechanistic target of rapamycin complex 1 (mTORC1) is an important mediator of pathological cardiac remodeling.

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Mechanisms of Copper-Induced Autophagy and Links with Human Diseases.

Pharmaceuticals (Basel)

January 2025

School of Pharmaceutical Sciences, Sun Yat-Sen University, Guangzhou 510006, China.

As a structural and catalytic cofactor, copper is involved in many biological pathways and is required for the biochemistry of all living organisms. However, excess intracellular copper can induce cell death due to its potential to catalyze the generation of reactive oxygen species, thus copper homeostasis is strictly regulated. And the deficiency or accumulation of intracellular copper is connected with various pathological conditions.

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