The recently discovered ferroptosis is a new kind of iron-regulated cell death that differs from apoptosis and necrosis. Ferroptosis can be induced by an oxidative stress response, a crucial pathological process implicated in cardiovascular diseases (CVDs). Accordingly, mounting evidence shows that oxidative stress-induced ferroptosis plays a pivotal role in angio-cardiopathy. To date, the inhibitors and activators of ferroptosis, as well as the many involved signaling pathways, have been widely explored. Among which, epigenetic regulators, molecules that modify the package of DNA without altering the genome, emerge as a highly targeted, effective option to modify the signaling pathway of ferroptosis and oxidative stress, representing a novel and promising therapeutic potential target for CVDs. In this review, we will briefly summarize the mechanisms of ferroptosis, as well as the role that ferroptosis plays in various CVDs. We will also expound the epigenetic regulators of oxidative stress-induced ferroptosis, and the promise that these molecules hold for treating the intractable CVDs.
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http://dx.doi.org/10.3389/fcell.2021.685775 | DOI Listing |
Appl Environ Microbiol
January 2025
Key Laboratory of Agricultural Environmental Microbiology, Ministry of Agriculture, Department of Microbiology, College of Life Sciences, Nanjing Agricultural University, Nanjing, Jiangsu, China.
Unlabelled: High temperature is an unavoidable environmental stress that generally exerts detrimental effects on organisms and has widespread effects on metabolism. Spermidine is an important member of the polyamines family and is involved in a range of abiotic stress responses in plants. Mitochondria play an essential role in cellular homeostasis and are key components of the stress response.
View Article and Find Full Text PDFIran J Basic Med Sci
January 2025
Biotechnology Research Center, Pharmaceutical Technology Institute, Mashhad University of Medical Sciences, Mashhad, Iran (Editor-in-Chief).
Objectives: This study aimed to determine the effect of 8-week high-intensity interval training (HIIT) on oxidative stress and apoptosis in the hippocampus of male rats with type 2 diabetes (T2D). The study focused on examining the role of proliferator-activated receptor gamma co-activator 1α (PGC1α)/Kelch-like ECH-associated protein Keap1/nuclear factor erythroid 2-related factor 2 (Nrf2) signaling pathway.
Materials And Methods: Twenty-eight 8-week-old Wistar rats were randomly assigned to one of four groups (n=7): control (Con), type 2 diabetes (T2D), exercise (Ex), and exercise + type 2 diabetes (Ex+T2D).
Front Immunol
January 2025
Division for Biochemistry of Joint and Connective Tissue Diseases, Department of Orthopedics, Ulm University Medical Center, Ulm, Germany.
Background: The complement system is locally activated after joint injuries and leads to the deposition of the terminal complement complex (TCC). Sublytic TCC deposition is associated with phenotypical alterations of human articular chondrocytes (hAC) and enhanced release of inflammatory cytokines. Chronic inflammation is a known driver of chondrosenescence in osteoarthritis (OA).
View Article and Find Full Text PDFFront Immunol
January 2025
Poultry Institute, Shandong Academy of Agricultural Science, Jinan, Shandong, China.
Heat-stress-induced oxidative and inflammatory responses were important factors contributing to chicken intestinal damage. The purpose of this study was based on the antioxidant and anti-inflammatory activities of Physalis Calyx seu Fructus (Jin Deng Long, JDL) to investigate its efficacy and mechanism in relieving chicken heat stress damage. Primary chicken embryo duodenum cells and 90 30-day-old specific-pathogen-free chicken were randomly divided into control and JDL groups to establish heat stress models and .
View Article and Find Full Text PDFFront Cardiovasc Med
January 2025
School of Life Sciences, Beijing University of Chinese Medicine, Beijing, China.
Cardiometabolic diseases (CMD) are leading causes of death and disability worldwide, with complex pathophysiological mechanisms in which inflammation plays a crucial role. This review aims to elucidate the molecular and cellular mechanisms within the inflammatory microenvironment of atherosclerosis, hypertension and diabetic cardiomyopathy. In atherosclerosis, oxidized low-density lipoprotein (ox-LDL) and pro-inflammatory cytokines such as Interleukin-6 (IL-6) and Tumor Necrosis Factor-alpha (TNF-α) activate immune cells contributing to foam cell formation and arterial wall thickening.
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