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The mitochondrial permeability transition (PT) is a well-recognized phenomenon that allows mitochondria to undergo a sudden increase of permeability to solutes with molecular mass ≤ 1500Da, leading to organelle swelling and structural modifications. The relevance of PT relies on its master role in the manifestation of programmed cell death (PCD). This function is performed by a mega-channel (in some cases inhibited by cyclosporin A) named permeability transition pore (PTP), whose function could derive from the assembly of different mitochondrial proteins. In this paper we examine the distribution and characteristics of PTP in mitochondria of eukaryotic organisms so far investigated in order to draw a hypothesis on the mechanism of its evolution. As a result, we suggest that PTP may have arisen as a new function linked to a multiple molecular exaptation of different mitochondrial proteins, even though they could nevertheless still play their original role. Furthermore, we suggest that the early appearance of PTP could have had a crucial role in the establishment of endosymbiosis in eukaryotic cells, by the coordinated balancing of ATP production by glycolysis (performed by the primary phagocyte) and oxidative phosphorylation (accomplished by the endosymbiont). Indeed, we argue on the possibility that this new energetic equilibrium could have opened the way to the subsequent evolution toward metazoans.
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http://dx.doi.org/10.1016/j.bbabio.2012.06.620 | DOI Listing |
Int J Numer Method Biomed Eng
September 2025
School of Mathematics and Statistics, University of Glasgow, Glasgow, UK.
Blood perfusion in cardiac tissues involves intricate interactions among vascular networks and tissue mechanics. Perfusion deficit is one of the leading causes of cardiac diseases, and modeling certain cardiac conditions that are clinically infeasible, invasive, or costly can provide valuable supplementary insights to aid clinicians. However, existing homogeneous perfusion models lack the complexity required for patient-specific simulations.
View Article and Find Full Text PDFInt J Biol Macromol
September 2025
Department of Nanoscience and Nanoengineering, Istanbul Technical University, 34469, Maslak, Istanbul, Turkey; Department of Chemistry, Faculty of Science and Letters, Istanbul Technical University, 34469, Maslak, Istanbul, Turkey. Electronic address:
This study presents the development of multifunctional starch-based biopolymer films reinforced with nitrogen-doped carbon quantum dots (N-CQDs), synthesized via a hydrothermal method, and exhibiting a high quantum yield (~70 %). N-CQDs were incorporated into the starch matrix at varying concentrations (0.1-1.
View Article and Find Full Text PDFFront Mol Neurosci
August 2025
Department of Cardiovascular Sciences, Lewis Katz School of Medicine, Lemole Center for Integrated Lymphatics and Vascular Research, Temple University, Philadelphia, PA, United States.
Introduction: Endothelial-to-mesenchymal transition (EndoMT), cell death, and fibrosis are increasingly recognized as contributing factors to Alzheimer's disease (AD) pathology, but the underlying transcriptomic mechanisms remain poorly defined. This study aims to elucidate transcriptomic changes associated with EndoMT, diverse cell death pathways, and fibrosis in AD using the 3xTg-AD mouse model.
Methods: Using RNA-seq data and knowledge-based transcriptomic analysis on brain tissues from the 3xTg-AD mouse model of AD.
Front Pharmacol
August 2025
AIMS BioScience, Co., Ltd., Seoul, Republic of Korea.
Introduction: Irinotecan (CPT-11), a topoisomerase I inhibitor, serves as a prodrug for SN-38, its active metabolite with significantly higher cytotoxic potency. Despite its clinical efficacy, irinotecan's therapeutic potential is limited by low fraction of conversion to SN-38, inefficient tumor targeting, and dose-limiting toxicities such as diarrhea and neutropenia. Nanoparticle-based formulations, such as SNB-101, offer a promising solution by encapsulating irinotecan and SN-38, enhancing solubility, improving drug delivery efficiency, and reducing systemic toxicity through tumor-specific accumulation via the enhanced permeability and retention (EPR) effect.
View Article and Find Full Text PDFEur J Pharmacol
September 2025
Department of Dermatology, the First Affiliated Hospital of Anhui Medical University, Hefei, Anhui, China; Key Laboratory of Dermatology (Anhui Medical University), Ministry of Education, Hefei, Anhui, China; Institute of Dermatology, Anhui Medical University, Hefei 230032, Anhui, China. Electronic
Vascular endothelial cells (ECs) damage is closely related to kidney injury. Our previous research revealed the involvement of interferon regulatory factor 1 (IRF1)-mediated PANoptosis of renal ECs in trichloroethylene (TCE)-induced immune kidney injury. However, how IRF1 regulates ECs PANoptosis remains unclear.
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