COVID-19 compromises iron homeostasis: Transferrin as a target of investigation

Gaiatto, Ana Carolina Macedo; Bibo, Thaciane Alkmim; Moreira, Nicolle de Godoy; Raimundo, Joyce Regina Santos; Alves, Beatriz da Costa Aguiar; Gascón, Thaís Moura; Carvalho, Samantha Sanches; Pereira, Edimar Cristiano; Fonseca, Fernando Luiz Affonso; Veiga, Gláucia Luciano da

doi:10.1016/j.jtemb.2022.127109

Cited by 6 publications

(4 citation statements)

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“…Hepcidin, in a regular expression, has a protective function against infections. However, its overexpression in COVID-19 can be detrimental and associated with various disease symptoms and a worse prognosis [ 88 , 89 ]. Hepcidin essentially downregulates FPN and therefore determines hypoferremia and iron sequestration at the cellular level [ 86 ].…”

Section: Ferroptosis and Covid-19mentioning

confidence: 99%

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Links between Vitamin K, Ferroptosis and SARS-CoV-2 Infection

et al. 2023

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Ferroptosis is a recently discovered form of programmed cell death. It is characterized by the accumulation of iron and lipid hydroperoxides in cells. Vitamin K is known to have antioxidant properties and plays a role in reducing oxidative stress, particularly in lipid cell membranes. Vitamin K reduces the level of reactive oxygen species by modulating the expression of antioxidant enzymes. Additionally, vitamin K decreases inflammation and potentially prevents ferroptosis. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection leading to coronavirus disease 2019 (COVID-19) is associated with oxidant–antioxidant imbalance. Studies have shown that intensified ferroptosis occurs in various tissues and cells affected by COVID-19. Vitamin K supplementation during SARS-CoV-2 infection may have a positive effect on reducing the severity of the disease. Preliminary research suggests that vitamin K may reduce lipid peroxidation and inhibit ferroptosis, potentially contributing to its therapeutic effects in COVID-19 patients. The links between ferroptosis, vitamin K, and SARS-CoV-2 infection require further investigation, particularly in the context of developing potential treatment strategies for COVID-19.

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Section: Ferroptosis and Covid-19mentioning

confidence: 99%

“…SARS-CoV-2 can probably imitate the action of hepcidin, increasing circulating and tissue FER. This induces serum iron deficiency and lowered hemoglobin [ 86 , 89 ]. It was noted that increased serum levels of hepcidin and FER are indeed associated with the severity of SARS-CoV-2 infection [ 92 ].…”

Section: Ferroptosis and Covid-19mentioning

confidence: 99%

Links between Vitamin K, Ferroptosis and SARS-CoV-2 Infection

et al. 2023

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“…Багатьом інфекційним агентам, включаючи вірус SARS-CoV-2, для реплікації та поширення потрібне залізо, що передбачає конкуренцію між господарем та вірусом. Результат цього змагання варіює час від часу, і залежить від багатьох факторів, таких як вік, стать, супутні захворювання та інші [24,25]. У разі інфікування COVID-19, організм обмежує доступ заліза від вірусу, накопичуючи його в клітинах за допомогою трансферинових рецепторів або гепсидину [24][25][26]…”

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“…Результат цього змагання варіює час від часу, і залежить від багатьох факторів, таких як вік, стать, супутні захворювання та інші [24,25]. У разі інфікування COVID-19, організм обмежує доступ заліза від вірусу, накопичуючи його в клітинах за допомогою трансферинових рецепторів або гепсидину [24][25][26]…”

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Long-COVID sequelae are associated with oxidative stress in hemodialysis patients

Stepanova

Korol

Snisar

et al. 2023

Ukr. J. Nephrol. and Dial.

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pathophysiology of long-COVID sequelae in the general population of SARS-CoV-2-infected patients has been shown to be strongly influenced by oxidative stress. However, the potential role of oxidative stress in the development of long-COVID sequelae in hemodialysis patients (HD) has never been investigated. The present study aimed to evaluate the oxidative status of HD patients 3.5 months after SARS-CoV-2 infection in relation to the presence of long-COVID sequelae and the severity of the acute phase COVID-19. Methods. This cross-sectional cohort study included 63 HD patients with a median age of 55 (43-62.5) years and a dialysis vintage of 42 (25-73) months who had been infected with COVID-19 at least 3 months before recruitment. Patients were divided into two groups according to the occurrence of long-COVID sequelae: Group 1 included 31 (49.2%) HD patients with sequelae, while Group 2 included 32 (50.8%) fully recovered individuals. At 3.5 (3.2-4.6) months after the acute phase of COVID-19, malondialdehyde (MDA) and erythrocyte levels (MDAe), sulfhydryl groups (SH -groups), serum catalase activity, transferrin, and ceruloplasmin were measured. A comparison of the obtained data was performed using the Student’s test or the Mann-Whitney test according to the data distribution. A correlation was evaluated with the Spearman test. Results. HD patients with persistent long-COVID sequelae had significantly higher concentrations of MDAs (p = 0.002), MDAe (p = 0.0006), and CTs (p = 0.02), and lower serum levels of SH-groups (p = 0.03) and ceruloplasmin (p = 0.03) compared with Group 2. The concentration of most studied indicators of pro- and antioxidant status did not depend on the severity of the acute phase COVID-19, and only catalase activity was statistically significantly related to the need for hospitalization (r = 0.59; p = 0.001), oxygen support (r = 0.44; p = 0.02), and the percentage of lung injury according to computed tomography (p = 0.03). Although the serum concentration of transferrin did not differ between the studied groups, the individual analysis showed that its value was statistically higher in HD patients with severe COVID-19 even 3.5 months after infection (p < 0.0001). Conclusions. Long-term COVID-19 sequelae in HD patients are associated with oxidative stress. High levels of catalase activity and serum transferrin 3.5 months after COVID-19 may be a consequence of the severe course of the acute phase of the disease. The obtained data suggest that the use of antioxidants may be one of the possible strategies to treat the long-term consequences of COVID in HD patients.

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Melatonin: a ferroptosis inhibitor with potential therapeutic efficacy for the post-COVID-19 trajectory of accelerated brain aging and neurodegeneration

Yehia,

Abulseoud

2024

Mol Neurodegeneration

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The unprecedented pandemic of COVID-19 swept millions of lives in a short period, yet its menace continues among its survivors in the form of post-COVID syndrome. An exponentially growing number of COVID-19 survivors suffer from cognitive impairment, with compelling evidence of a trajectory of accelerated aging and neurodegeneration. The novel and enigmatic nature of this yet-to-unfold pathology demands extensive research seeking answers for both the molecular underpinnings and potential therapeutic targets. Ferroptosis, an iron-dependent cell death, is a strongly proposed underlying mechanism in post-COVID-19 aging and neurodegeneration discourse. COVID-19 incites neuroinflammation, iron dysregulation, reactive oxygen species (ROS) accumulation, antioxidant system repression, renin-angiotensin system (RAS) disruption, and clock gene alteration. These events pave the way for ferroptosis, which shows its signature in COVID-19, premature aging, and neurodegenerative disorders. In the search for a treatment, melatonin shines as a promising ferroptosis inhibitor with its repeatedly reported safety and tolerability. According to various studies, melatonin has proven efficacy in attenuating the severity of certain COVID-19 manifestations, validating its reputation as an anti-viral compound. Melatonin has well-documented anti-aging properties and combating neurodegenerative-related pathologies. Melatonin can block the leading events of ferroptosis since it is an efficient anti-inflammatory, iron chelator, antioxidant, angiotensin II antagonist, and clock gene regulator. Therefore, we propose ferroptosis as the culprit behind the post-COVID-19 trajectory of aging and neurodegeneration and melatonin, a well-fitting ferroptosis inhibitor, as a potential treatment.

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COVID-19 compromises iron homeostasis: Transferrin as a target of investigation

Cited by 6 publications

References 20 publications

Links between Vitamin K, Ferroptosis and SARS-CoV-2 Infection

Links between Vitamin K, Ferroptosis and SARS-CoV-2 Infection

Long-COVID sequelae are associated with oxidative stress in hemodialysis patients

Melatonin: a ferroptosis inhibitor with potential therapeutic efficacy for the post-COVID-19 trajectory of accelerated brain aging and neurodegeneration

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