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    Combating sars-cov-2 through lipoxins, proteasome, caveolin and nuclear factor-?b pathways in non-pregnant and pregnant populations
    (NLM (Medline), 2020) Çelik, Önder; Çelik, Nilüfer; Aydın, Süleyman; Baysal, Bora; Aydın, Suna; Sa?lam, Aylin; Gürsu, Yağmur; Dalkılıç, Semih; Ulaş, Mustafa; Özçil, Mustafa Doğan; Tayyar, Ahter Tanay; Cengiz, Ferhat; Uğur, Kader; Akkoç, Ramazan Fazıl; Erşahin, Aynur Adeviye
    It can be misleading to think that the new severe acute respiratory syndrome coronavirus (SARS-CoV2) which has a very strong mutation and adaptation capabilities, uses only the angiotensin-converting enzyme II (ACE2) pathway to reach target cells. Despite all the precautions taken, the pandemic attack continues and the rapid increase in the number of deaths suggest that this virus has entered the cell through different pathways and caused damage through different mechanisms. The main reason why the ACE2 pathway comes to the fore in all scientific studies is that this receptor is located at the entry point of basic mechanisms that provide alveolo-capillary homeostasis. SARS-CoV-2 has to use nuclear factor-?B (NF-kB), caveloae, clathrin, lipoxin, serine protease and proteasome pathways in addition to ACE2 to enter the target cell and initiate damage. For this reason, while new drug development studies are continuing, in order to be beneficial to patients in their acute period, it is imperative that we are able to come up with drugs that activate or inhibit these pathways and are currently in clinical use. It is also critical that we adopt these new pathways to the treatment of pregnant women affected by SARS-CoV-2, based on the scientific data we use to treat the general population.
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    Factors preventing materno-fetal transmission of SARS-CoV-2
    (W.B. Saunders Ltd, 2020) Çelik, Önder; Sa?lam, Aylin; Baysal, Bora; Derwig, Iris E.; Çelik, Nilüfer; Ak, Mehmet; Aslan, Selma Nergis; Ulaş, Mustafa; Erşahin, Aynur Adeviye; Duran, Bülent; Aydın, Süleyman
    Although many pregnant women have been infected by coronavirus, the presence of intrauterine vertical transmission has not been conclusively reported yet. What prevents this highly contagious virus from reaching the fetus? Is it only the presence of a strong placental barrier, or is it the natural absence of the some receptor that the viruses use for transmission? We, therefore, need to comprehensively understand the mechanism of action of the mammalian epithelial barriers located in two different organs with functional similarity. The barriers selected as potential targets by SARS-CoV-2 are the alveolo-capillary barrier (ACB), and the syncytio-capillary barrier (SCB). Caveolae are omega-shaped structures located on the cell membrane. They consist of caveolin-1 protein (Cav-1) and are involved in the internalisation of some viruses. By activating leukocytes and nuclear factor-?B, Cav-1 initiates inflammatory reactions. The presence of more than one Cav-1 binding sites on coronavirus is an important finding supporting the possible relationship between SARS-CoV-2-mediated lung injury. While the ACB cells express Cav-1 there is no caveolin expression in syncytiotrophoblasts. In this short review, we will try to explain our hypothesis that the lack of caveolin expression in the SCB is one of the most important physiological mechanisms that prevents vertical transmission of SARS-CoV-2. Since the physiological Cav-1 deficiency appears to prevent acute cell damage treatment algorithms could potentially be developed to block this pathway in the non-pregnant population affected by SARS-CoV-2.