The novel coronavirus disease 2019 (COVID-19) is a rapidly expanding infection around the world. The world Health Organization (WHO) in March 2020 announced the Coronavirus pandemic. This infection causes many deaths on daily basis. Therapeutic options are currently limited. It is revealed that COVID-19 binds to human angiotensin-converting enzyme 2 (ACE2) to enter the host cells. One of the activities of ACE2 is hydrolyzing the active bradykinin metabolite [des-Arg973] BK (DABK). A decreased activity or reducing expression of ACE2 by the virus impairs the inactivation of DABK. This enhances its signaling through the bradykinin B1 receptor (BKB1R) and could lead to fluid extravasation and leukocyte recruitment to the lung. Targeting the bradykinin system by either blocking the bradykinin production or blocking bradykinin receptors may open a new potential therapeutic window for the treatment of COVID-19 induced acute respiratory distress syndrome (ARDS) particularly before patients enter the irreversible stages.
Renal ischemia-reperfusion (RIR) is a pathological condition due to transient restriction of blood flow to the kidneys, which is followed by the subsequent recovery of perfusion and re-oxygenation. RIR injury contributes to the progression of renal dysfunction including acute kidney injury (AKI) in native and renal allograft transplant. The generation of reactive oxygen species (ROS) during oxidative stress contributes to the occurrence of RIR. Hence, the use of antioxidant compounds can improve oxidative stress due to RIR. This review highlights herbal antioxidant efficacy against RIR injury. The findings of this study indicate that antioxidant compounds with herbal origin could reduce complications due to oxidative stress related to RIR through diminishing lipid peroxidation, decreased production of malondialdehyde (MDA), apoptosis and increasing antioxidant enzymes activity. Reducing oxidative stress with the pharmacological approach of antioxidants can be a desirable target for ameliorating RIR.
Male gender is an obvious risk factor for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection and mortality rate is higher in men than women. Undoubtedly, gender-related behavioral factors, such as higher amounts of smoking, alcohol consumption, and biological differences in immune systems could make males more vulnerable. The role of androgen-responsive elements (AREs) of transmembrane serine proteases type II (TMPRSS2) gene as one of the major players of male dominancy in severe COVID-19 infection has been under appreciated and needs to be clarified.
MYH9-related diseases (MYH9-RD) are clinically represented by thrombocytopenia, large platelets, proteinuria and various degrees of renal dysfunction. We present a 25-year-old male with thrombocytopenia, large platelets, renal dysfunction and proteinuria. Gene sequencing of whole exons of MYH9 gene confirmed the diagnosis of MYH9-related disorder and revealed single nucleotide polymorphisms (SNPs) in the introns 13 (rs3752462) and 14 (rs2413396) and a mutation in exon 26 of MYH9 gene. Our result supported the possibility of non-coding SNPs involvement in the pathogenicity of the MYH9-RD disease and successful renal transplant in this patient.
COVID-19 cell entry via Non-Endosomal pathway: A host Serine protease (TMPRSS2) is responsible for priming the spikes and allows the virus entry via non-endosomal pathway. Cleavage at S1-S2 junction by TMPRSS2 activates membrane fusion. Bromhexine Hydrochloride is shown to act as a bioavailable inhibitor of TMPRSS2.
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