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Study on the Synergistic Effect of Klotho and KRAS on Reducing Ferroptosis After Myocardial Infarction by Regulating RAP1/ERK Signaling Pathway.

Appl Biochem Biotechnol

January 2025

Department of Internal Medicine-Cardiovascular, Guangzhou Twelfth People's Hospital, No.1, Tianqiang Road, Tianhe District, Guangzhou City, Guangdong Province, 510620, China.

Myocardial infarction (MI) is a coronary artery-related disease that seriously threatens human life and is the leading cause of sudden death worldwide, where a lack of nutrients and oxygen leads to an inflammatory response and death of cardiomyocytes. Ferroptosis is a form of non-apoptotic cell death associated with metabolic dysfunction, resulting in abnormal breakdown of glutamine and iron-dependent accumulation of reactive oxygen species (ROS) during metabolism. However, the molecular mechanism of ferroptosis in the pathogenesis of MI and the function of Klotho and KRAS on ferroptosis during MI remain unclear.

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De novo root regeneration (DNRR) involves activation of special cells after wounding, along with the converter cells, reactive oxygen species, ethylene, and jasmonic acid, also playing key roles. An updated DNRR model is presented here with gene regulatory networks. Root formation after tissue injury is a type of plant regeneration known as de novo root regeneration (DNRR).

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Mitochondria represent pivotal cellular organelles endowed with multifaceted functionalities encompassing cellular respiration, metabolic processes, calcium turnover, and the regulation of apoptosis, primarily through the generation of reactive oxygen species (ROS). Perturbations in mitochondrial dynamics have been intricately linked to the etiology of numerous cardiovascular pathologies, such as heart failure, ischemic heart disease, and various cardiomyopathies. Notably, recent attention has been directed towards the detrimental impact of micro- and nanoplastic pollution on mitochondrial integrity, an area underscored by a paucity of comprehensive investigations.

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Disproportion between reactive oxygen species (ROS) production and the body's antioxidant system can cause oxidative stress, which is considered a common denominator in various pathological conditions, including cardiovascular diseases, aging, and cognitive disorders. The generation of free radicals, which occurs through partial reduction of oxygen, can quickly overwhelm the endogenous antioxidant system capacity of the cell. This causes lipid, protein, DNA and RNA damage, inflammation, and overall cell degeneration, which can be mitigated by various antioxidants.

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Dietary Compounds in the Prevention of Arsenic Induced Intestinal Toxicity .

J Med Food

January 2025

Instituto de Agroquímica y Tecnología de Alimentos (IATA-CSIC), Paterna (Valencia), Spain.

Recent studies show that inorganic arsenic (As) exerts a toxic effect on the intestinal epithelium, causing a significant increase in its permeability. This disruption of the epithelial barrier may favor the entry of contaminants or toxins into the systemic circulation, thus causing toxicity not only at the intestinal level but possibly also at the systemic level. The present study conducts an evaluation of the protective effect of various dietary supplements and plant extracts against the intestinal toxicity of inorganic As.

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