Association of Circadian Clock and Severe Acute Respiratory Syndrome Coronavirus 2 Infection

Tomar, Renu; Raghav, Alok

doi:10.33069/cim.2021.0010

Chronobiol Med

2021

DOI: 10.33069/cim.2021.0010

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Association of Circadian Clock and Severe Acute Respiratory Syndrome Coronavirus 2 Infection

Renu Tomar

Alok Raghav

Abstract: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is causing devastation worldwide accounting millions of deaths. This virus is among the new member of the Coronaviridae family with differences from SARS-CoV. The entry of the virus to human cells mediated through spike (S) proteins with angiotensin-converting enzyme 2 (ACE2). Several comorbidities such as hypertension, diabetes, HIV, malignancy, diabetes, chronic respiratory disease, and cardiovascular disease makes a person susceptible to COVID-19 … Show more

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Cited by 3 publications

References 41 publications

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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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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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A Study on Chronofatality Trends of COVID-19 Deaths at a Tertiary Care Hospital

et al. 2021

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The aim of the study is to find out any association between time of death in coronavirus disease (COVID-19) patients and variables like age, sex, and existence of comorbidities including type II diabetes mellitus, hypertension, coronary artery disease, chronic kidney disease, etc. An attempt was also made to elucidate the reasons for relationship between time of death and other aforementioned variables. Mortality data of 1,553 COVID-19 cases from a tertiary care hospital between March 2020 to September 2021 were analyzed. Maximum deaths occurred between 18:01 hours to 06:00 hours of the 24-hour cycle. There is a significant statistical association between time of death and age, time of death and sex, time of death and having a comorbidity of diabetes mellitus in the study sample. The study confirms that the chronofatality of COVID-19 deaths has a nocturnal predilection. The circadian rhythms of glucocorticoids, respiratory physiology of sleep, and circadian hemodynamic variations may have a role in prognosis and fatality of COVID-19.

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Could Timed Targeting of the Circadian-Controlled NLRP3 Inflammasome Be a Potential Therapeutic Strategy for Treatment of COVID-19–Induced Encephalitis?

Chukwunyere

2024

Chronobiol Med

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The new coronavirus disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has several manifestations including neurological complications like encephalitis. The NOD-like receptor family pyrin domain-containing 3 (NLRP3) inflammasomes, which are regulated by the circadian clock genes, are key signaling proteins that detect pathogenic microorganisms and sterile stressors and activate the pro-inflammatory cytokines such as interleukin-1β and -18 (IL-1β and IL-18). The disruption of circadian rhythms following SARS-CoV-2 binding to angiotensin-converting enzyme 2 (ACE2) receptors in the capillary endothelium could lead to hyperactivation of the NLRP3 inflammasome, contributing to an enhanced inflammatory response in the central nervous system, thereby increasing susceptibility to or severity of coronavirus disease 2019 (COVID-19)-induced encephalitis. This review highlights the role of the circadian-controlled NLRP3 inflammasome in the pathogenesis of COVID-19-induced encephalitis and suggests targeting the NLRP3 circadian axis for timely intervention as a potential therapeutic target for the treatment of COVID-19-induced encephalitis.

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Association of Circadian Clock and Severe Acute Respiratory Syndrome Coronavirus 2 Infection

Cited by 3 publications

References 41 publications

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

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

A Study on Chronofatality Trends of COVID-19 Deaths at a Tertiary Care Hospital

Could Timed Targeting of the Circadian-Controlled NLRP3 Inflammasome Be a Potential Therapeutic Strategy for Treatment of COVID-19–Induced Encephalitis?

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