Abstract Ferroptosis, a regulated form of cellular death characterized by the iron-mediated accumulation of lipid peroxides, provides a novel avenue for delving into the intersection of cellular metabolism, oxidative stress, and disease pathology. We have witnessed a mounting fascination with ferroptosis, attributed to its pivotal roles across diverse physiological and pathological conditions including developmental processes, metabolic dynamics, oncogenic pathways, neurodegenerative cascades, and traumatic tissue injuries. By unraveling the intricate underpinnings of the molecular machinery, pivotal contributors, intricate signaling conduits, and regulatory networks governing ferroptosis, researchers aim to bridge the gap between the intricacies of this unique mode of cellular death and its multifaceted implications for health and disease. In light of the rapidly advancing landscape of ferroptosis research, we present a comprehensive review aiming at the extensive implications of ferroptosis in the origins and progress of human diseases. This review concludes with a careful analysis of potential treatment approaches carefully designed to either inhibit or promote ferroptosis. Additionally, we have succinctly summarized the potential therapeutic targets and compounds that hold promise in targeting ferroptosis within various diseases. This pivotal facet underscores the burgeoning possibilities for manipulating ferroptosis as a therapeutic strategy. In summary, this review enriched the insights of both investigators and practitioners, while fostering an elevated comprehension of ferroptosis and its latent translational utilities. By revealing the basic processes and investigating treatment possibilities, this review provides a crucial resource for scientists and medical practitioners, aiding in a deep understanding of ferroptosis and its effects in various disease situations. 

The mechanism of ferroptosis and its related diseases

Ferroptosis is a novel form of cell death caused by the accumulation of lipid peroxides in an iron-dependent manner. However, the precise mechanism underlying the exploitation of ferroptosis by influenza A viruses (IAV) remains unclear. The results demonstrate that IAV promotes its own replication through ferritinophagy by sensitizing cells to ferroptosis, with hemagglutinin identified as a key trigger in this process. Hemagglutinin interacts with autophagic receptors nuclear receptor coactivator 4 (NCOA4) and tax1-binding protein 1 (TAX1BP1), facilitating the formation of ferritin-NCOA4 condensates and inducing ferritinophagy. Further investigation shows that hemagglutinin-induced ferritinophagy causes cellular lipid peroxidation, inhibits aggregation of mitochondrial antiviral signaling protein (MAVS), and suppresses the type I interferon response, thereby contributing to viral replication. Collectively, a novel mechanism by which IAV hemagglutinin induces ferritinophagy resulting in cellular lipid peroxidation, consequently impairing MAVS-mediated antiviral immunity, is revealed. 

The Hemagglutinin of Influenza A Virus Induces Ferroptosis to Facilitate Viral Replication

Ferroptosis is a novelty form of regulated cell death, and it is mainly characterized by iron accumulation and lipid peroxidation in the cells. Its underlying mechanism is related to the amino acid, iron, and lipid metabolisms. During viral infection, pathogenic microorganisms have evolved to interfere with ferroptosis, and ferroptosis is often manipulated by viruses to regulate host cell servicing for viral reproduction. Therefore, this review provides a comprehensive overview of the mechanisms underlying ferroptosis, elucidates the intricate signaling pathways involved, and explores the pivotal role of ferroptosis in the pathogenesis of viral infections. By enhancing our understanding of ferroptosis, novel therapeutic strategies can be devised to effectively prevent and treat diseases associated with this process. Furthermore, unraveling the developmental mechanisms through which viral infections exploit ferroptosis will facilitate development of innovative antiviral agents.

Molecular Mechanisms of Ferroptosis and Its Role in Viral Pathogenesis

Background The pain and sleep disorders caused by arthritis are health issues that have been re-emphasized with the aging population. However, the majority of research on arthritis and sleep disorders has focused on cases that have already been diagnosed with arthritis. This research aims to explore the correlation between sleep duration and new-onset arthritis in middle-aged and older adult individuals. Methods Utilizing data from the China Health and Retirement Longitudinal Study from baseline (2011) to the Wave 3 follow-up (2018), we conducted a 7-year longitudinal investigation targeting populations with valid sleep questionnaire records and without arthritis. Sleep duration was assessed from nighttime sleep and daytime nap records. The new-onset of arthritis was determined based on self-reported diagnosis. We employed different logistic regression models to consider the potential impact of sleep duration on arthritis and conducted mediation analyses to assess the involvement of BMI in the association between sleep duration and the new-onset risk of arthritis. Results Out of the 6,597 individuals analyzed in the cohort, 586 (8.9%) were diagnosed with new-onset arthritis. Median sleep duration was notably shorter in the new-onset arthritis group (6.63 vs. 6.41 h, p &amp;lt; 0.05). There was a notable negative correlation found between new-onset risk of arthritis and sleep duration, with each Interquartile Range (IQR) increment in sleep leading to a 16% risk reduction (OR: 0.864; 95% CI: 0.784–0.954). Stratified analyses revealed BMI as a potential modifier in the sleep-arthritis relationship ( P for interaction = 0.05). Mediation analyses further showed that about 3.5% of the association was mediated by BMI. Additionally, the inclusion of sleep duration improved the arthritis predictive power of our model, with an IDI of 0.105 (0.0203, 0.1898) and an NRI of 0.0013 (0.0004, 0.0022) after adding sleep duration to the basic model. Conclusion In the middle-aged and older adult demographic of China, increased sleep duration is associated with a decreased new-onset risk of arthritis, with BMI potentially playing a role in mediating this connection. 

pdf/sleep-duration-and-the-risk-of-new-onset-arthritis-in-middle-5145szmo7t.pdf

Sleep duration and the risk of new-onset arthritis in middle-aged and older adult population: results from prospective cohort study in China

Background Our previous studies have shown that the basic helix-loop-helix family member e40 (Bhlhe40) plays a critical role in regulating calcification and senescence of vascular smooth muscle cells induced by high glucose. In this study, we determined the association between serum Bhlhe40 levels and subclinical atherosclerosis in patients with type 2 diabetes mellitus (T2DM). Methods 247 patients with T2DM were included in this cross-sectional study between June 2021 and July 2022. The presence of subclinical atherosclerosis was evaluated by carotid ultrasonography. Serum Bhlhe40 concentrations were measured with an ELISA kit. Results Serum Bhlhe40 levels were remarkably higher in the subclinical atherosclerosis group than in the subjects without subclinical atherosclerosis (p < 0.001). Correlation analysis showed a positive correlation between serum Bhlhe40 and carotid intima-media thickness (C-IMT) (r = 0.155, p = 0.015). The optimal threshold of serum Bhlhe40 > 5.67 ng/mL had an area under the ROC curve (AUC) was 0.709 (p < 0.001). In addition, serum Bhlhe40 levels were associated with the prevalence of subclinical atherosclerosis (OR: 1.790, 95% CI: 1.414–2.266, p < 0.001). Conclusion Serum Bhlhe40 levels were significantly higher in T2DM subjects with subclinical atherosclerosis and positively associated with C-IMT.

https://doi.org/10.1177/14791641231169246

High serum Bhlhe40 levels are associated with subclinical atherosclerosis in patients with type 2 diabetes mellitus: A cross-sectional study

H1N1 influenza virus infection through NRF2-KEAP1-GCLC pathway induces ferroptosis in nasal mucosal epithelial cells.

Obstructive sleep apnea-increased DEC1 regulates systemic inflammation and oxidative stress that promotes development of pulmonary arterial hypertension

Hearing loss, as a sensory disorder, is the most common occurrence among humans, which has received increasing attention from society. It is mainly caused by the damage of inner ear hair cells (HCs) or the degeneration of spiral ganglion neurons. In mammals, cochlear HCs cannot regenerate naturally after injury, leading to irreversible hearing loss. Therefore, HCs are essential for hearing protection. In recent years, the protection of drug-related ototoxicity, inner ear stem cells, gene therapy, new materials, and signal regulation have become important ways to develop regeneration strategies of HCs. An in-depth study of the causes of the occurrence and development of hearing impairment and the regeneration of hearing loss for effective prevention, discovery, and treatment of deafness has great significance. This review aimed to analyze the development of the inner ear and summarize the related factors leading to HCs injury and the research progress of regeneration after injury. 

Development of the inner ear and regeneration of hair cells after hearing impairment

Synergy of 5-Aminolevulinate Supplement and CX3CR1 Suppression Promotes Liver Regeneration via M2 Macrophage-Derived IGF-1

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H1N1 influenza virus infection through NRF2-KEAP1-GCLC pathway induces ferroptosis in nasal mucosal epithelial cells.

Obstructive sleep apnea-increased DEC1 regulates systemic inflammation and oxidative stress that promotes development of pulmonary arterial hypertension

Development of the inner ear and regeneration of hair cells after hearing impairment

Synergy of 5-Aminolevulinate Supplement and CX3CR1 Suppression Promotes Liver Regeneration via M2 Macrophage-Derived IGF-1