Dysregulated Bradykinin: Mystery in the Pathogenesis of COVID-19

Tabassum, Aisha; Iqbal, Mohammad; Sultan, Sadia; Alhuthali, Raghad Ali; Alshubaili, Deena Ismail; Sayyam, Raghad Salah; Abyad, Lama Mohammed; Qasem, Ahmed; Arbaeen, Ahmad F.

doi:10.1155/2022/7423537

Cited by 19 publications

(13 citation statements)

References 39 publications

(104 reference statements)

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“…A system linked to RAS is the kallikrein-kinin-system (KKS) since ACE and ACE2 are regulators for degradation pathways within this system. The KKS is upregulated in inflammation and induces an increase in bradykinin via cleavage of kininogens by kallikrein ( 24 ). Bradykinin can bind to bradykinin2-receptor (B2R), which leads to vasodilatation and decreased blood pressure, thus serving as a natural counterbalancing system to RAS.…”

Section: Two Sides Of the Same Evil - Sars-cov-2 And Its Vaccinesmentioning

confidence: 99%

The rationale for the treatment of long-Covid symptoms – A cardiologist's view

Schieffer

2022

Front. Cardiovasc. Med.

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The ongoing coronavirus disease 2019 pandemic left us with thousands of patients suffering from neurological, cardiovascular, and psychiatric disorders named post-acute sequelae of COVID-19 or just long-Covid. In parallel, the vaccination campaigns against SARS-CoV-2 spike protein saved millions of lives worldwide but long-Covid symptoms also appeared rarely following vaccination with a strong overlap to the “canonical” long-Covid symptoms. A therapeutic strategy targeting both, post-VAC and post-SARS-CoV-2 long-Covid symptoms is warranted since exposure to the S-protein either by vaccination or SARS-CoV-2 infection may trigger identical immuno-inflammatory cascades resulting in long-Covid symptoms.

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Section: Two Sides Of the Same Evil - Sars-cov-2 And Its Vaccinesmentioning

confidence: 99%

The rationale for the treatment of long-Covid symptoms – A cardiologist's view

Schieffer

2022

Front. Cardiovasc. Med.

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“…RAAS system dysfunction may instigate the cytokine storm in COVID-19. Accordingly, SARS-CoV-2-mediated inhibition of ACE2 may result in increased availability of diverse molecules that are associated with hyper-inflammatory response, hence leading to COVID-19 progression 89 .…”

Section: Sars-cov-2-mediated Raas System Dysfunctionmentioning

confidence: 99%

Pyroptotic cell death in SARS-CoV-2 infection: revealing its roles during the immunopathogenesis of COVID-19

Wang¹,

Chang²,

Zhang³

et al. 2022

Int. J. Biol. Sci.

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The rapid dissemination of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the causative agent of coronavirus disease 2019 , remains a global public health emergency. The host immune response to SARS-CoV-2 plays a key role in COVID-19 pathogenesis. SARS-CoV-2 can induce aberrant and excessive immune responses, leading to cytokine storm syndrome, autoimmunity, lymphopenia, neutrophilia and dysfunction of monocytes and macrophages. Pyroptosis, a proinflammatory form of programmed cell death, acts as a host defense mechanism against infections. Pyroptosis deprives the replicative niche of SARS-CoV-2 by inducing the lysis of infected cells and exposing the virus to extracellular immune attack. Notably, SARS-CoV-2 has evolved sophisticated mechanisms to hijack this cell death mode for its own survival, propagation and shedding. SARS-CoV-2-encoded viral products act to modulate various key components in the pyroptosis pathways, including inflammasomes, caspases and gasdermins. SARS-CoV-2-induced pyroptosis contriubtes to the development of COVID-19-associated immunopathologies through leakage of intracellular contents, disruption of immune system homeostasis or exacerbation of inflammation. Therefore, pyroptosis has emerged as an important mechanism involved in COVID-19 immunopathogenesis. However, the entangled links between pyroptosis and SARS-CoV-2 pathogenesis lack systematic clarification. In this review, we briefly summarize the characteristics of SARS-CoV-2 and COVID-19-related immunopathologies. Moreover, we present an overview of the interplay between SARS-CoV-2 infection and pyroptosis and highlight recent research advances in the understanding of the mechanisms responsible for the implication of the pyroptosis pathways in COVID-19 pathogenesis, which will provide informative inspirations and new directions for further investigation and clinical practice. Finally, we discuss the potential value of pyroptosis as a therapeutic target in COVID-19. An in-depth discussion of the underlying mechanisms of COVID-19 pathogenesis will be conducive to the identification of potential therapeutic targets and the exploration of effective treatment measures aimed at conquering SARS-CoV-2-induced COVID-19.

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“…Increased expression of ACE2 could prove to be of therapeutic benefit in COVID-19 infection. Commonly used RAS-modulating pharmacological agents such as ACEi increase ACE2 levels, whereas the use of ARBs causes an increase in the expression and activity levels of ACE and ACE2 [ 33 , 34 ]. Increased ACE2 might be useful in the late stages of infection to counteract the hyperinflammatory and hyperphybrotic state of lung tissue.…”

Section: Pharmacological Approach On Ace2mentioning

confidence: 99%

Pharmacotherapy Based on ACE2 Targeting and COVID-19 Infection

Vitiello¹,

Ferrara²

2022

IJMS

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The new SARS-CoV-2 coronavirus is responsible for the COVID-19 pandemic. A massive vaccination campaign, which is still ongoing, has averted most serious consequences worldwide; however, lines of research are continuing to identify the best drug therapies to treat COVID-19 infection. SARS-CoV-2 penetrates the cells of the host organism through ACE2. The ACE2 protein plays a key role in the renin–angiotensin system (RAS) and undergoes changes in expression during different stages of COVID-19 infection. It appears that an unregulated RAS is responsible for the severe lung damage that occurs in some cases of COVID-19. Pharmacologically modifying the expression of ACE2 could be an interesting line of research to follow in order to avoid the severe complications of COVID-19.

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Dysregulated Bradykinin: Mystery in the Pathogenesis of COVID-19

Cited by 19 publications

References 39 publications

The rationale for the treatment of long-Covid symptoms – A cardiologist's view

The rationale for the treatment of long-Covid symptoms – A cardiologist's view

Pyroptotic cell death in SARS-CoV-2 infection: revealing its roles during the immunopathogenesis of COVID-19

Pharmacotherapy Based on ACE2 Targeting and COVID-19 Infection

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