WITHDRAWN: Common NLRP3 inflammasome inhibitors and Covid-19: Divide and Conquer

Batiha, Gaber El‐Saber; Al-Gareeb, Ali I; Qusti, Safaa; Alshammari, Eida M.; Rotimi, Damilare; Adeyemi, Oluyomi Stephen; Al-Kuraishy, Hayder M

doi:10.1016/j.sciaf.2021.e01084

Cited by 26 publications

(37 citation statements)

References 70 publications

(60 reference statements)

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“…Of note, both of NF-κB and NLRP3 inflammasome persuade asymmetry of erythrocyte membrane with decrease of erythrocyte deformability in normal and sickle erythrocytes (52,53). Besides, NF-κB and NLRP3 inflammasome are extremely triggered in COVID-19 (54), and might a latent causes for lessening of erythrocyte deformability in COVID-19.…”

Section: Hyperviscosity Syndrome and Inflammatory Signaling Pathways ...mentioning

confidence: 96%

Changes in the Blood Viscosity in Patients With SARS-CoV-2 Infection

et al. 2022

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Coronavirus disease 2019 (COVID-19) is caused by a novel virus known as severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). SARS-CoV-2-induced hyperinflammation together with alteration of plasma proteins, erythrocyte deformability, and platelet activation, may affect blood viscosity. Thus, this review aimed to study the link between SARS-CoV-2 infection and alteration of blood viscosity in COVID-19 patients. In order to review findings related to hyperviscosity in COVID-19, we suggested a protocol for narrative review of related published COVID-19 articles. Hyperviscosity syndrome is developed in different hematological disorders including multiple myeloma, sickle cell anemia, Waldenstorm macroglobulinemia, polycythemia, and leukemia. In COVID-19, SARS-CoV-2 may affect erythrocyte morphology via binding of membrane cluster of differentiation 147 (CD147) receptors, and B and 3 proteins on the erythrocyte membrane. Variations in erythrocyte fragility and deformability with endothelial dysfunction and oxidative stress in SARS-CoV-2 infection may cause hyperviscosity syndrome in COVID-19. Of interest, hyperviscosity syndrome in COVID-19 may cause poor tissue perfusion, peripheral vascular resistance, and thrombosis. Most of the COVID-19 patients with a blood viscosity more than 3.5 cp may develop coagulation disorders. Of interest, hyperviscosity syndrome is more commonly developed in vaccine recipients who had formerly received the COVID-19 vaccine due to higher underlying immunoglobulin concentrations, and only infrequently in those who have not received the COVID-19 vaccine. Taken together, these observations are untimely too early to give a final connotation between COVID-19 vaccination and the risk for development of hyperviscosity syndrome, consequently prospective and retrospective studies are necessary in this regard.

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Section: Hyperviscosity Syndrome and Inflammatory Signaling Pathways ...mentioning

confidence: 96%

Changes in the Blood Viscosity in Patients With SARS-CoV-2 Infection

et al. 2022

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“…Both of NF-κB and NLRP3 inflammasome induce asymmetry of RBCs membrane with reduction of RBCs deformability in normal and sickle RBCs [ 45 , 46 ]. In addition, NF-κB and NLRP3 inflammasome are highly activated in COVID-19 [ 47 ] and could a potential causes for reduction of RBCs deformability in COVID-19.…”

Section: Hyperviscosity Syndrome and Covid-19mentioning

confidence: 99%

Hyperviscosity syndrome in COVID-19 and related vaccines: exploring of uncertainties

et al. 2022

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Hyperviscosity syndrome (HVS) recently emerged as a complication of coronavirus disease 2019 (COVID-19) and COVID-19 vaccines. Therefore, the objectives of this critical review are to establish the association between COVID-19 and COVID-19 vaccines with the development of HVS. HVS may develop in various viral infections due to impairment of humoral and cellular immunity with elevation of immunoglobulins. COVID-19 can increase blood viscosity (BV) through modulation of fibrinogen, albumin, lipoproteins, and red blood cell (RBC) indices. HVS can cause cardiovascular and neurological complications in COVID-19 like myocardial infarction (MI) and stroke. HVS with or without abnormal RBCs function in COVID-19 participates in the reduction of tissue oxygenation with the development of cardio-metabolic complications and long COVID-19. Besides, HVS may develop in vaccine recipients with previous COVID-19 due to higher underlying Ig concentrations and rarely without previous COVID-19. Similarly, patients with metabolic syndrome are at the highest risk for propagation of HVS after COVID-19 vaccination. In conclusion, COVID-19 and related vaccines are linked with the development of HVS, mainly in patients with previous COVID-19 and underlying metabolic derangements. The possible mechanism of HVS in COVID-19 and related vaccines is increasing levels of fibrinogen and immunoglobulins. However, dehydration, oxidative stress, and inflammatory reactions are regarded as additional contributing factors in the pathogenesis of HVS in COVID-19. However, this critical review cannot determine the final causal relationship between COVID-19 and related vaccines and the development of HVS. Prospective and retrospective studies are warranted in this field.

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“…Indeed, SARS-CoV-2 infection triggers activation of nod-like receptor pyrin 3 (NLRP3) inflammasome with subsequent stimulation of immune cells, TLR4/NF-κB axis and pro-inflammatory cytokine release [ 62 ]. These changes linked NLRP3 inflammasome activation with development of cytokine storm and sever systemic inflammation.…”

Section: Fenofibrate and Covid-19mentioning

confidence: 99%

“…These changes linked NLRP3 inflammasome activation with development of cytokine storm and sever systemic inflammation. Thus, inhibitors of NLRP3 inflammasome could be beneficial against immune over-activation-induced hyperinflammation and development of cytokine storm in COVID-19 [ 62 ]. Of note, fenofibrate had ability to mitigate diabetic retinopathy by inhibiting activation of NLRP3 inflammasome in mice with experimental diabetes [ 63 ].…”

Section: Fenofibrate and Covid-19mentioning

confidence: 99%

Fenofibrate for COVID-19 and related complications as an approach to improve treatment outcomes: the missed key for Holy Grail

et al. 2022

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Introduction Fenofibrate is an agonist of peroxisome proliferator activated receptor alpha (PPAR-α), that possesses anti-inflammatory, antioxidant, and anti-thrombotic properties. Fenofibrate is effective against a variety of viral infections and different inflammatory disorders. Therefore, the aim of critical review was to overview the potential role of fenofibrate in the pathogenesis of SARS-CoV-2 and related complications. Results By destabilizing SARS-CoV-2 spike protein and preventing it from binding angiotensin-converting enzyme 2 (ACE2), a receptor for SARS-CoV-2 entry, fenofibrate can reduce SARS-CoV-2 entry in human cells Fenofibrate also suppresses inflammatory signaling pathways, which decreases SARS-CoV-2 infection-related inflammatory alterations. In conclusion, fenofibrate anti-inflammatory, antioxidant, and antithrombotic capabilities may help to minimize the inflammatory and thrombotic consequences associated with SARSCoV-2 infection. Through attenuating the interaction between SARS-CoV-2 and ACE2, fenofibrate can directly reduce the risk of SARS-CoV-2 infection. Conclusions As a result, fenofibrate could be a potential treatment approach for COVID-19 control.

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WITHDRAWN: Common NLRP3 inflammasome inhibitors and Covid-19: Divide and Conquer

Cited by 26 publications

References 70 publications

Changes in the Blood Viscosity in Patients With SARS-CoV-2 Infection

Changes in the Blood Viscosity in Patients With SARS-CoV-2 Infection

Hyperviscosity syndrome in COVID-19 and related vaccines: exploring of uncertainties

Fenofibrate for COVID-19 and related complications as an approach to improve treatment outcomes: the missed key for Holy Grail

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