The role of ferroptosis in metabolic diseases DOI Creative Commons
Ling Xie, Bin Fang, Chun Zhang

et al.

Biochimica et Biophysica Acta (BBA) - Molecular Cell Research, Journal Year: 2023, Volume and Issue: 1870(6), P. 119480 - 119480

Published: April 30, 2023

Language: Английский

Resolution of inflammation via RvD1/FPR2 signaling mitigates Nox2 activation and ferroptosis of macrophages in experimental abdominal aortic aneurysms DOI
Amanda C. Filiberto, Zachary Ladd, Victoria Leroy

et al.

The FASEB Journal, Journal Year: 2022, Volume and Issue: 36(11)

Published: Oct. 2, 2022

Abstract Abdominal aortic aneurysm (AAA) formation is characterized by inflammation, leukocyte infiltration, and vascular remodeling. Resolvin D1 (RvD1) derived from ω‐3 polyunsaturated fatty acids involved in the resolution phase of chronic inflammatory diseases. The aim this study was to decipher protective role RvD1 via formyl peptide receptor 2 (FPR2) signaling attenuating abdominal aneurysms (AAA). elastase‐treatment model AAA C57BL/6 (WT) mice human tissue used confirm our hypotheses. Elastase‐treated FPR2 −/− had a significant increase diameter, proinflammatory cytokine production, immune cell infiltration (macrophages neutrophils), elastic fiber disruption, decrease smooth muscle α‐actin expression compared elastase‐treated WT mice. treatment attenuated formation, remodeling mice, but not Importantly, demonstrated significantly decreased mRNA non‐aneurysm aortas. Mechanistically, RvD1/FPR2 mitigated p47 phox phosphorylation prevented hallmarks ferroptosis, such as lipid peroxidation Nrf2 translocation, thereby HMGB1 secretion. Collectively, demonstrates RvD1‐mediated immunomodulation on macrophages mitigate ferroptosis release, leading inflammation during pathogenesis.

Language: Английский

Citations

32

The Selenoprotein Glutathione Peroxidase 4: From Molecular Mechanisms to Novel Therapeutic Opportunities DOI Open Access

Kamari Weaver,

Rachid Skouta

Published: Feb. 24, 2022

The selenoprotein glutathione peroxidase 4 (GPX4) is one of the main antioxidant mediators in human body. Its central function involves reduction complex hydroperoxides into their respective alcohols often using reduced Glutathione (GSH) as a reducing agent. GPX4 has become hotspot therapeutic target biomedical research following its characterization chief regulator ferroptosis, and subsequent recognition specific pharmacological for treatment an extensive variety diseases including cancers neurodegenerative disorders. Several recent studies have provided insights how distinguished from rest family, unique biochemical properties GPX4, related to lipid peroxidation enzyme may be modulated potential target. This current report aims review literature underlying all these present up-to-date perspective on understanding

Language: Английский

Citations

29

Curcumin Attenuates Periodontal Injury via Inhibiting Ferroptosis of Ligature-Induced Periodontitis in Mice DOI Open Access
Yawei Wang, Hongbing Lin, Wenxin Huang

et al.

International Journal of Molecular Sciences, Journal Year: 2023, Volume and Issue: 24(12), P. 9835 - 9835

Published: June 7, 2023

Periodontitis is a chronic infectious disease characterized by the destruction of connective tissue and alveolar bone that eventually leads to tooth loss. Ferroptosis an iron-dependent regulated cell death involved in ligature-induced periodontitis vivo. Studies have demonstrated curcumin has potential therapeutic effect on periodontitis, but mechanism still unclear. The purpose this study was investigate protective effects alleviating ferroptosis periodontitis. Ligature-induced periodontal-diseased mice were used detect curcumin. level superoxide dismutase (SOD), malondialdehyde (MDA) total glutathione (GSH) gingiva assayed. Furthermore, mRNA expression levels acsl4, slc7a11, gpx4 tfr1 measured using qPCR protein ACSL4, SLC7A11, GPX4 TfR1 investigated Western blot immunocytochemistry (IHC). Curcumin reduced MDA increased GSH. Additionally, proven significantly increase SLC7A11 inhibit ACSL4 TfR1. In conclusion, plays role inhibiting mice.

Language: Английский

Citations

20

Ferroptosis in cardiac hypertrophy and heart failure DOI Open Access
K. Zhang,

Xin-Miao Tian,

Wei Li

et al.

Biomedicine & Pharmacotherapy, Journal Year: 2023, Volume and Issue: 168, P. 115765 - 115765

Published: Oct. 24, 2023

Heart failure has become a public health problem that we cannot avoid choosing to face in today's context. In the case of heart failure, pathological cardiac hypertrophy plays major role because its condition absolute increase ventricular mass under various stresses. Ferroptosis, it could be defined as regulatory mechanisms regulate cell death absence apoptosis iron-dependent cells. This paper introduces new research findings on use different cellular ferroptosis for treatment and hypertrophy, providing therapeutic targets directions clinical treatment. The mechanism field been increasingly demonstrated, relationship between which is one causes also an area should focus on. addition, latest applications progress inducers inhibitors are reported this paper, updating breakthroughs their fields.

Language: Английский

Citations

19

The role of ferroptosis in metabolic diseases DOI Creative Commons
Ling Xie, Bin Fang, Chun Zhang

et al.

Biochimica et Biophysica Acta (BBA) - Molecular Cell Research, Journal Year: 2023, Volume and Issue: 1870(6), P. 119480 - 119480

Published: April 30, 2023

Language: Английский

Citations

18