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Mechanisms of cognitive impairment associated with cerebral infarction.
Zhong Nan Da Xue Xue Bao Yi Xue Ban
October 2024
Department of Neurology, Second Xiangya Hospital, Central South University, Changsha 410011, China.
Cerebral infarction is a common type of stroke with high incidence and disability rates, and most patients experience varying degrees of cognitive impairment. The manifestations and severity of post-infarction cognitive impairment are influenced by multiple interacting factors, and its pathophysiological mechanisms are highly complex, involving pericyte degeneration, excessive generation of reactive oxygen species (ROS), overproduction of glutamate, and overactivation of autophagy. After cerebral infarction, abnormal pericyte function activates neuroinflammation and facilitates the entry of inflammatory mediators into the brain; detachment of pericytes from blood vessels disrupts the integrity of the blood-brain barrier.
View Article and Find Full Text PDFMLKL as an emerging machinery for modulating organelle dynamics: regulatory mechanisms, pathophysiological significance, and targeted therapeutics.
Front Pharmacol
February 2025
School of Pharmacy, Nantong University, Nantong, Jiangsu, China.
Mixed lineage kinase domain-like protein (MLKL) is a pseudokinase featured by a protein kinase-like domain without catalytic activity. MLKL was originally discovered to be phosphorylated by receptor-interacting protein kinase 1/3, typically increase plasma membrane permeabilization, and disrupt the membrane integrity, ultimately executing necroptosis. Recent evidence uncovers the association of MLKL with diverse cellular organelles, including the mitochondrion, lysosome, endosome, endoplasmic reticulum, and nucleus.
View Article and Find Full Text PDFCellular homeostatic responses to lysosomal damage.
Trends Cell Biol
March 2025
Center for Global Health, Department of Internal Medicine, University of New Mexico Health Sciences Center, Albuquerque, NM 87106, USA; Autophagy, Inflammation, and Metabolism Center of Biochemical Research Excellence, Albuquerque, NM 87106, USA.
Lysosomes are essential membrane-bound organelles that control cellular homeostasis by integrating intracellular functions with external signals. Their critical roles make lysosomal membranes vulnerable to rupture under various stressors, leading to cellular dysfunction. However, the mechanisms by which cells respond to lysosomal damage have only recently begun to be explored.
View Article and Find Full Text PDFNobiletin-mediated autophagy mitigates nanoplastic-induced toxicity in human intestinal Caco-2 cells.
FASEB J
March 2025
Department of Food and Nutrition, College of BioNano Technology, Gachon University, Seongnam-si, Republic of Korea.
The presence of nanoplastics (NPs), which cause oxidative stress and damage to the cell structure due to the breakdown of microplastics (MPs), poses considerable ecological and health challenges. This study investigated the protective role of nobiletin (NOB), a flavonoid derived from citrus peel, in modulating autophagy and mitigating NP-induced toxicity in human intestinal Caco-2 cells. The Caco-2 cells were treated with NPs and varying concentrations of NOB to evaluate cell viability, apoptosis, and autophagic activity.
View Article and Find Full Text PDFCKLF1 disrupts microglial efferocytosis following acute ischemic stroke by binding to phosphatidylserine.
Cell Death Differ
March 2025
Shenzhen Hospital of Integrated Traditional Chinese and Western Medicine, Shenzhen Clinical College of Integrated Chinese and Western Medicine, Guangzhou University of Chinese Medicine, Shenzhen, China.
Efferocytosis is crucial for the clearance of apoptotic cells (ACs) following acute ischemic stroke (AIS), however, its mechanism remains unclear. This study reveals that chemokine-like factor 1 (CKLF1) disrupts efferocytosis by promoting AC finding and internalization while impairing AC degradation in microglia. CKLF1 deficiency reduced the proportion of ACs and lowered levels of damage-associated molecular patterns.
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