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Molecular Research of Endocytic and Autophagic Pathways in Diseases

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: 20 February 2025 | Viewed by 2472

Special Issue Editors


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Guest Editor
1. i3S-Instituto de Investigação e Inovação em Saúde, Universidade do Porto, 4200-135 Porto, Portugal
2. Department of Neurosciences, Santa Maria Health School, 4049-024 Porto, Portugal
Interests: oncobiology; adrenocortical tumors; anticancer drugs; cancer drug resistance; cancer biomarkers; extracellular vesicles; intracellular trafficking pathways; endocytic pathway; endosomal-lysosomal system; autophagy; programmed cell death

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Co-Guest Editor
1. Unit for Multidisciplinary Research in Biomedicine (UMIB), 4050-346 Porto, Portugal
2. Instituto de Ciências Biomédicas Abel Salazar, University of Porto, 4099-002 Porto, Portugal
Interests: adrenocortical tumors; obesity; bariatric surgery; signaling pathways

Special Issue Information

Dear Colleagues,

Different membrane trafficking pathways such as recycling, lysosomal or autophagic pathways are essential for cellular homeostasis. Therefore, alterations in the regulation of those intracellular trafficking routes have been associated with different pathologies including cancer, neurological disorders and metabolic diseases. Endocytic pathways play a pivotal role, since the endosome is a dynamic organelle, which is involved in the sorting of cargo for recycling, for degradation or even for the biogenesis of extracellular vesicles.

This Special Issue of International Journal of Molecular Sciences aims to bring together state-of-the-art original research and reviews on the molecular research of autophagic and endocytic pathways in diseases. Topics may include the study of the: i) paradoxical role of autophagy in diseases, ii) interdependency of intracellular trafficking routes, and iii) autophagic or endocytic players as potential biomarkers of disease. Articles on the development of new methodologies to assess the status of these intracellular trafficking pathways will also be considered.

Dr. Diana Sousa
Dr. Sofia S. Pereira
Guest Editors

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Keywords

  • autophagy
  • endocytic pathway
  • endosome
  • multivesicular body
  • autophagosome endosomal–lysosomal system
  • extracellular vesicles
  • intracellular trafficking pathways
  • membrane fusion
  • metabolism

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Published Papers (1 paper)

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Research

13 pages, 1326 KiB  
Communication
Autophagy Markers Are Altered in Alzheimer’s Disease, Dementia with Lewy Bodies and Frontotemporal Dementia
by Antonio Longobardi, Marcella Catania, Andrea Geviti, Erika Salvi, Elena Rita Vecchi, Sonia Bellini, Claudia Saraceno, Roland Nicsanu, Rosanna Squitti, Giuliano Binetti, Giuseppe Di Fede and Roberta Ghidoni
Int. J. Mol. Sci. 2024, 25(2), 1125; https://doi.org/10.3390/ijms25021125 - 17 Jan 2024
Viewed by 1777
Abstract
The accumulation of protein aggregates defines distinct, yet overlapping pathologies such as Alzheimer’s disease (AD), dementia with Lewy bodies (DLB), and frontotemporal dementia (FTD). In this study, we investigated ATG5, UBQLN2, ULK1, and LC3 concentrations in 66 brain specimens and 120 plasma samples [...] Read more.
The accumulation of protein aggregates defines distinct, yet overlapping pathologies such as Alzheimer’s disease (AD), dementia with Lewy bodies (DLB), and frontotemporal dementia (FTD). In this study, we investigated ATG5, UBQLN2, ULK1, and LC3 concentrations in 66 brain specimens and 120 plasma samples from AD, DLB, FTD, and control subjects (CTRL). Protein concentration was measured with ELISA kits in temporal, frontal, and occipital cortex specimens of 32 AD, 10 DLB, 10 FTD, and 14 CTRL, and in plasma samples of 30 AD, 30 DLB, 30 FTD, and 30 CTRL. We found alterations in ATG5, UBQLN2, ULK1, and LC3 levels in patients; ATG5 and UBQLN2 levels were decreased in both brain specimens and plasma samples of patients compared to those of the CTRL, while LC3 levels were increased in the frontal cortex of DLB and FTD patients. In this study, we demonstrate alterations in different steps related to ATG5, UBQLN2, and LC3 autophagy pathways in DLB and FTD patients. Molecular alterations in the autophagic processes could play a role in a shared pathway involved in the pathogenesis of neurodegeneration, supporting the hypothesis of a common molecular mechanism underlying major neurodegenerative dementias and suggesting different potential therapeutic targets in the autophagy pathway for these disorders. Full article
(This article belongs to the Special Issue Molecular Research of Endocytic and Autophagic Pathways in Diseases)
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