Potential role of lipoxin in the management of COVID-19: a narrative review

Batiha, Gaber El‐Saber; Al-Gareeb, Ali I; Elekhnawy, Engy; Al-Kuraishy, Hayder M

doi:10.1007/s10787-022-01070-3

Cited by 32 publications

(25 citation statements)

References 81 publications

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“…In vitro study observed that SRT-1720 was not toxic to cell lines. Recently, SRT-1720 was effective in AD through the modulation of mitochondrial autophagy and biogenesis via the SIRT1-dependent pathway (Shukla et al 2016 ; Batiha et al 2022 ). Therefore, SRT-1720, through activation of SIRT1, could be a promising future therapy in the management of PD.…”

Section: Role Of Sirt1 Activators In Pdmentioning

confidence: 99%

SIRT1 pathway in Parkinson’s disease: a faraway snapshot but so close

et al. 2022

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Silent information regulator (SIRT) has distinctive enzymatic activities and physiological functions to control cell-cycle progression, gene expression, and DNA stability by targeting histone and non-histone proteins. SIRT1 enhances synaptic formation and synaptic activity, and therefore, can reduce the progression of various degenerative brain diseases including Parkinson’s disease (PD). SIRT1 activity is decreased by aging with a subsequent increased risk for the development of degenerative brain diseases. Inhibition of SIRT1 promotes inflammatory reactions since SIRT1 inhibits transcription of nuclear factor kappa B (NF-κB) which also inhibits SIRT1 activation via activation of microRNA and miR-34a which reduce NAD synthesis. SIRT1 is highly expressed in microglia as well as neurons, and has antioxidant and anti-inflammatory effects. Therefore, this review aimed to find the possible role of SIRT1 in PD neuropathology. SIRT1 has neuroprotective effects; therefore, downregulation of SIRT1 during aging promotes p53 expression and may increase the vulnerability of neuronal cell deaths. PD neuropathology is linked with the sequence of inflammatory changes and the release of pro-inflammatory cytokines due to the activation of inflammatory signaling pathways. In addition, oxidative stress, inflammatory disorders, mitochondrial dysfunction, and apoptosis contribute mutually to PD neuropathology. Thus, SIRT1 and SIRT1 activators play a crucial role in the mitigation of PD neuropathology through the amelioration of oxidative stress, inflammatory disorders, mitochondrial dysfunction, apoptosis, and inflammatory signaling pathways.

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Section: Role Of Sirt1 Activators In Pdmentioning

confidence: 99%

SIRT1 pathway in Parkinson’s disease: a faraway snapshot but so close

et al. 2022

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“…The fusion protein of the SARS‐CoV‐2 spike protein is enhanced by Ca 2+. 59,60 These findings suggest that Ca 2+ is necessary for binding, entry and invasion of SARS‐CoV‐2. SARS‐CoV‐2 entry is associated with activation of endosomal Ca 2+ channels, which are necessary for uptake of SARS‐CoV‐2.…”

Section: Role Of Ryanodine Receptors and Dantrolene In Covid‐19mentioning

confidence: 91%

Dantrolene and ryanodine receptors in COVID‐19: The daunting task and neglected warden

Alkazmi

Al-Kuraishy

Al-Gareeb

et al. 2023

Clin Exp Pharma Physio

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Dantrolene (DTN) is a ryanodine receptor (RyR) antagonist that inhibits Ca 2+ release from stores in the sarcoplasmic reticulum. DTN is mainly used in the management of malignant hyperthermia. RyRs are highly expressed in immune cells and are involved in different viral infections, including severe acute respiratory syndrome coronavirus type 2 (SARS-CoV-2), because Ca 2+ is necessary for viral replication, maturation and release. DTN can inhibit the proliferation of SARS-CoV-2, indicating its potential role in reducing entry and pathogenesis of SARS-CoV-2. DTN may increase clearance of SARS-CoV-2 and promote coronavirus disease 2019 (COVID-19) recovery by shortening the period of infection. DTN inhibits N-methyl-D-aspartate (NMDA) mediated platelets aggregations and thrombosis. Therefore, DTN may inhibit thrombosis and coagulopathy in COVID-19 through suppression of platelet NMDA receptors. Moreover, DTN has a neuroprotective effect against SARS-CoV-2 infection-induced brain injury through modulation of NMDA receptors, which are involved in excitotoxicity, neuronal injury and the development of neuropsychiatric disorders. In conclusion, DTN by inhibiting RyRs may attenuate inflammatory disorders in SARS-CoV-2 infection and associated cardio-pulmonary complications. Therefore, DNT could be a promising drug therapy against COVID-19. Preclinical and clinical studies are warranted in this regards.

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“…Maresin1 and its epoxide intermediate 13S, 14S-epoxi-DHA, enhance the macrophage conversion from M1 to M2 phenotype, it is well known that M2 are pro-resolving in nature, enhance macrophage phagocytosis and efferocytosis ( Freedman et al, 2020 ). Lipoxins (LXs) might reduce the inflammatory changes that occur due to activation of MAPK, mTOR, and NLPR3 inflammasome in COVID-19, reduce tumor necrosis factor-alpha and interferon-gamma secretion, block T cell migration and promote T cell apoptosis ( Batiha et al, 2022 ). Neuroprotectin D1/Protectin reduce PMN infiltration through endothelial cells and stimulate the removal of apoptotic cells by MΦ t have crucial hereby play a crucial role in managing diseases such as Alzheimer’s disease ( Rajasagi et al, 2013 ; Mohammed et al, 2022 ).…”

Section: Spms In Regulation Of Inflammatory Macrophages In Covid-19mentioning

confidence: 99%

“…Lipoxins (LXs), can inhibition of viral entry and its replication, downregulate ACE2 receptors, inhibit release of the pro-inflammatory cytokines. Moreover, LXs can augment the polarization of macrophages from (M1) to (M2) phenotype, causing a shift from pro-inflammatory to anti-inflammatory environment, thereby enhancing the inflammation resolving actions of macrophages in SARS-CoV-2 infection ( Das, 2021 ; Batiha et al, 2022 ). RvE1and RvE4 enhances macrophage phagocytosis and efferocytosis of senescent erythrocytes that characterize COVID-19 ( Libreros et al, 2021 ).…”

Section: Spms In Regulation Of Inflammatory Macrophages In Covid-19mentioning

confidence: 99%

Specialized pro-resolving lipid mediators regulate inflammatory macrophages: A paradigm shift from antibiotics to immunotherapy for mitigating COVID-19 pandemic

Kumar

Yasmeen²,

Chaudhary³

et al. 2023

Front. Mol. Biosci.

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The most severe clinical manifestations of the horrifying COVID-19 disease, that claimed millions of lives during the pandemic time, were Acute respiratory distress syndrome (ARDS), Coagulopathies, septic shock leading eventually to death. ARDS was a consequence of Cytokine storm. The viral SARS-COV2infection lead to avalanche of cytokines and eicosanoids causing “cytokine storm” and “eicosanoid storm.” Cytokine storm is one of the macrophage-derived inflammatory responses triggered by binding of virus particles to ACE2 receptors of alveolar macrophages, arise mainly due to over production of various pro-inflammatory mediators like cytokines, e.g., interleukin (IL)-1, IL-2, and tumor necrosis factor (TNF)- α, causing pulmonary edema, acute respiratory distress, and multi-organ failure. Cytokine storm was regarded as the predictor of severity of the disease and was deemed one of the causes of the high mortality rates due to the COVID-19. The basis of cytokine storm is imbalanced switching between an inflammation increasing - pro-inflammatory (M1) and an inflammation regulating-anti-inflammatory (M2) forms of alveolar macrophages which further deteriorates if opportunistic secondary bacterial infections prevail in the lungs. Lack of sufficient knowledge regarding the virus and its influence on co-morbidities, clinical treatment of the diseases included exorbitant use of antibiotics to mitigate secondary bacterial infections, which led to the unwarranted development of multidrug resistance (MDR) among the population across the globe. Antimicrobial resistance (AMR) needs to be addressed from various perspectives as it may deprive future generations of the basic health immunity. Specialized pro-resolving mediators (SPMs) are generated from the stereoselective enzymatic conversions of essential fatty acids that serve as immune resolvents in controlling acute inflammatory responses. SPMs facilitate the clearance of injured tissue and cell debris, the removal of pathogens, and augment the concentration of anti-inflammatory lipid mediators. The SPMs, e.g., lipoxins, protectins, and resolvins have been implicated in exerting inhibitory influence on with cytokine storm. Experimental evidence suggests that SPMS lower antibiotic requirement. Therefore, in this review potential roles of SPMs in enhancing macrophage polarization, triggering immunological functions, hastening inflammation resolution, subsiding cytokine storm and decreasing antibiotic requirement that can reduce AMR load are discussed.

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Potential role of lipoxin in the management of COVID-19: a narrative review

Cited by 32 publications

References 81 publications

SIRT1 pathway in Parkinson’s disease: a faraway snapshot but so close

SIRT1 pathway in Parkinson’s disease: a faraway snapshot but so close

Dantrolene and ryanodine receptors in COVID‐19: The daunting task and neglected warden

Specialized pro-resolving lipid mediators regulate inflammatory macrophages: A paradigm shift from antibiotics to immunotherapy for mitigating COVID-19 pandemic

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