PANoptosis and cardiovascular disease: The preventive role of exercise training.

Regulated cell death, including pyroptosis, apoptosis, and necroptosis, is vital for the body's defense system. Recent research suggests that these three types of cell death are interconnected, giving rise to a new concept called PANoptosis. PANoptosis has been linked to various diseases, making it crucial to comprehend its mechanism for effective treatments. PANoptosis is controlled by upstream receptors and molecular signals, which form polymeric complexes known as PANoptosomes. Cell death combines necroptosis, apoptosis, and pyroptosis and cannot be fully explained by any of these processes alone. Understanding pyroptosis, apoptosis, and necroptosis is essential for understanding PANoptosis. Physical exercise has been shown to suppress pyroptotic, apoptotic, and necroptotic signaling pathways by reducing inflammatory factors, proapoptotic factors, and necroptotic factors such as caspases and TNF-alpha. This ultimately leads to a decrease in cardiac structural remodeling. The beneficial effects of exercise on cardiovascular health may be attributed to its ability to inhibit these cell death pathways.

Cuproptosis and physical training: A review.

Copper is an essential element in the human body, involved in many physiological and metabolic functions, including coagulation, oxidative metabolism, and hormone production. The maintenance of copper homeostasis within cells is a complex procedure that is intrinsically controlled by a multitude of intricate mechanisms. Disorders of copper homeostasis encompass a wide range of pathological conditions, including degenerative neurological diseases, metabolic disorders, cardio-cerebrovascular diseases, and tumors. Cuproptosis, a recently identified non-apoptotic mode of cell death mode, is characterized by copper dependence and the regulation of mitochondrial respiration. Cuproptosis represents a novel form of cell death distinct from the previously described modes, including apoptosis, necrosis, pyroptosis, and ferroptosis. Excess copper has been shown to induce cuproptosis by stimulating protein toxic stress responses via copper-dependent abnormal oligomerization of lipoylation proteins within the tricarboxylic acid cycle and the subsequent reduction of iron-sulfur cluster protein levels. Ferredoxin1 facilitates the lipoacylation of dihydrolipoyl transacetylase, which in turn degrades iron-sulfur cluster proteins by reducing Cu2+ to Cu+, thereby inducing cell death. Furthermore, copper homeostasis is regulated by the copper transporter, and disturbances in this homeostasis result in cuproptosis. Current evidence suggests that cuproptosis plays an important role in the onset and development of several cardiovascular diseases. Copper-chelating agents, including ammonium tetrathiomolybdate (VI) and DL-penicillamine, have been shown to facilitate the alleviation of cardiovascular disease by inhibiting cuproptosis. It is hypothesized that oxidative phosphorylation inhibitors such as physical training may inhibit cuproptosis by inhibiting the protein stress response. In conclusion, the implementation of physical training may be a viable strategy to reducte the incidence of cuproptosis.

Ferroptosis and aerobic training in ageing.

 Ferroptosis is a form of programmed cell death that plays a significant role in causing several diseases such as heart attack and heart failure, through alterations in fat, amino acid, and iron metabolism. Comprehending the regulatory mechanisms of ferroptosis signaling is critical because it has a considerable effect on the elderly's mortality. Conversely, age-related changes in substrate metabolism and metabolite levels are recognized to give rise to obesity. Furthermore, research has proposed that aging and obesity-related changes in substrate metabolism may aggravate ferroptosis. The suppression of ferroptosis holds potential as a successful therapeutic approach for managing different diseases, including sarcopenia, cardiovascular diseases, and central nervous system diseases. However, the pathologic and biological mechanisms behind the function of ferroptosis are not fully comprehended yet. Physical activity could affect lipid, amino acid, and iron metabolism to modulate ferroptosis. The aim of this study is to showcase the current understanding of the molecular mechanisms leading to ferroptosis and discuss the role of aging and physical activity in this phenomenon.

An alginate-based eutectogel impregnated with polyvinylpyrrolidone/benzoic acid deep eutectic solvent and magnetic carboxylated multiwalled carbon nanotubes: Evaluated as sorbent in green microextraction of pesticides.

This article presents the synthesis and application of a novel magnetic eutectogel constituting a polymeric deep eutectic solvent (PDES), carboxylated multiwall carbon nanotube (MWCNT-COOH), and super-dispersible/super-paramagnetic polyvinylpyrrolidone coated-Fe3O4 nanocrystals incorporated in alginate gel. Different methods were used for the characterization of novel polymeric based DES gel including FT-NMR, ATR-FTIR, and SEM were used. The novel DES eutectogel was used for the extraction of pesticides from honey. The modified eutectogel with PDES, MWCNT, and PDES-MWCNT showed 1.8-, 1.4-, and 2.5-fold enhancement in the sorption efficiency under green magnetic micro-solid-phase extraction (MSPE) method before GC-MS analysis. Important factors including the acidity of the samples, adsorption and desorption conditions, and the ionic strength of the preparation solution were investigated. The matrix effect, specificity, the quantification limits (0.023-1.023 µg kg-1), linear dynamic range (0.023-500 µg kg-1 with R2 of 0.9845-0.9986), relative standard deviations (<8.4%), were evaluated. In addition, the method was used to analyze 12 pesticides in four samples of honey. In the spiked concentration range of 0.1 to 10 µg kg-, the obtained recoveries were between 73.2 and 110.8% (RSD% = 8.1%, n = 3).