Epilepsy is a disease characterized by recurrent, episodic, and transient central nervous system (CNS) dysfunction resulting from an excessive synchronous discharge of brain neurons. It is characterized by diverse etiology, complex pathogenesis, and difficult treatment. In addition, most epileptic patients exhibit social cognitive impairment and psychological impairment. Iron is an essential trace element for human growth and development and is also involved in a variety of redox reactions in organisms. However, abnormal iron metabolism is associated with several neurological disorders, including hemorrhagic post-stroke epilepsy and post-traumatic epilepsy (PTE). Moreover, ferroptosis is also considered a new form of regulation of cell death, which is attributed to severe lipid peroxidation caused by the production of reactive oxygen species (ROS) and iron overload found in various neurological diseases, including epilepsy. Therefore, this review summarizes the study on iron metabolism and ferroptosis in epilepsy, in order to elucidate the correlation between iron and epilepsy. It also provides a novel method for the treatment, prevention, and research of epilepsy, to control epileptic seizures and reduce nerve injury after the epileptic seizure.
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http://dx.doi.org/10.3389/fnins.2020.601193 | DOI Listing |
Nat Commun
December 2024
Department of Biomedicine, Aarhus University, 8000, Aarhus C, Denmark.
CD163, a macrophage-specific receptor, plays a critical role in scavenging hemoglobin released during hemolysis, protecting against oxidative effects of heme iron. In the bloodstream, hemoglobin is bound by haptoglobin, leading to its immediate endocytosis by CD163. While haptoglobin's structure and function are well understood, CD163's structure and its interaction with the haptoglobin-hemoglobin complex have remained elusive.
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December 2024
Shenzhen Institute of Synthetic Biology, Shenzhen Institutes of Advanced Technology, Chinese Academy of Sciences, Shenzhen, 518055, China.
Iron is a potent biochemical, and accurate homeostatic control is orchestrated by a network of interacting players at multiple levels. Although our understanding of organismal iron homeostasis has advanced, intracellular iron homeostasis is poorly understood, including coordination between organelles and iron export into the ER/Golgi. Here, we show that SLC39A13 (ZIP13), previously identified as a zinc transporter, promotes intracellular iron transport and reduces intracellular iron levels.
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December 2024
Key Laboratory of Urban Pollutant Conversion, Institute of Urban Environment, Chinese Academy of Sciences, Xiamen, China.
The emergence of single-atom catalysts offers exciting prospects for the green production of hydrogen peroxide; however, their optimal local structure and the underlying structure-activity relationships remain unclear. Here we show trace Fe, up to 278 mg/kg and derived from microbial protein, serve as precursors to synthesize a variety of Fe single-atom catalysts containing FeNO (1 ≤ x ≤ 4) moieties through controlled pyrolysis. These moieties resemble the structural features of nonheme Fe-dependent enzymes while being effectively confined on a microbe-derived, electrically conductive carbon support, enabling high-current density electrolysis.
View Article and Find Full Text PDFEcol Lett
January 2025
Center for Reservoir and Aquatic System Research, Baylor University, Waco, Texas, USA.
Diazotrophic cyanobacteria can overcome nitrogen (N)-limitation by fixing atmospheric N; however, this increases their energetic, iron, molybdenum, and boron costs. It is unknown how current and historic N-supplies affect cyanobacterial elemental physiology beyond increasing demands for elements involved in N-fixation. Here, we examined the changes in pigment concentrations, N-storage, and the ionome (i.
View Article and Find Full Text PDFFront Immunol
December 2024
Critical Care Department, Hebei General Hospital, Shijiazhuang, Hebei, China.
Ischemia-reperfusion injuries (IRI) across various organs and tissues, along with sepsis, significantly contribute to the progression of critical illnesses. These conditions disrupt the balance of inflammatory mediators and signaling pathways, resulting in impaired physiological functions in human tissues and organs. Ferroptosis, a distinct form of programmed cell death, plays a pivotal role in regulating tissue damage and modulating inflammatory responses, thereby influencing the onset and progression of severe illnesses.
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