scholarly journals A Correlation among the COVID-19 Spread, Particulate Matters, and Angiotensin-Converting Enzyme 2: A Review

2021 ◽  
Vol 2021 ◽  
pp. 1-8
Author(s):  
Zafran Khan ◽  
Daniya Ualiyeva ◽  
Asaf Khan ◽  
Nasib Zaman ◽  
Sanjeep Sapkota ◽  
...  

Air pollution (AP) is one of the leading causes of health risks because it causes widespread morbidity and mortality every year. Its impact on the environment includes acid rain and decreased visibility, but more importantly, it also has an impact on human health. The rise of COVID-19 demonstrates the cost of failing to manage AP. COVID-19 can be spread through the air, and atmospheric particulate matters (PMs) can create a good atmosphere for the long-distance spread of the virus. Moreover, these PMs can cause lung cell inflammation, thereby increasing sensitivity and the severity of symptoms in COVID-19 patients. In this study, we emphasized the potential role of PMs in the spread of COVID-19. The relationship among COVID-19, PMs, and angiotensin-converting enzyme 2 (ACE2) (receptor involved in virus entry into lung cells and inflammation) was also summarized.

2020 ◽  
Vol 9 (2) ◽  
pp. 78-85
Author(s):  
Malyn M.L.K. Antoine ◽  
Yancheng Xu ◽  
Rimanatou Seyni-Boureima ◽  
Chrystal Deniza Antoine-Frank ◽  
Coumba Aicha Thiam ◽  
...  

COVID-19, caused by the severe acute respiratory syndrome coronavirus (SARS-CoV-2), was first identified in China in late 2019 and since then, this disease has become a pandemic affecting many countries across the globe. Due to this outbreak, many researchers have been diligently investigating this disease for the establishment of better methods of its treatment and control. Evidence from research has led to a plethora of valuable but uncertain information on the modes of transmission of COVID-19 and the mechanisms by which SARS-CoV-2 establishes infections in targeted tissues. It is now better understood that in this disease, SARS-CoV-2 gains entrance into cells by specifically binding ACE-2 (angiotensin-converting enzyme 2); ACE-2 serves as a potential receptor for the virus. The lungs, in addition to many other organs and tissues, express ACE-2 in varying degrees. Therefore, this review will examine the role of ACE-2 in COVID-19 and the secondary effects that COVID-19 has on organs that express ACE-2. To this end, it will assist in establishing the relationship between the ACE-2 receptor and SARS-CoV-2, bringing to the forefront the correlation between the symptomatology presentation, as well as the severity of infections experienced with COVID-19. Given this, it may even provide an avenue for the generation of treatment, or create a platform for the enhanced knowledge of this novel virus, and therefore, control, and maybe unravel the mystery for long term complications.  


2020 ◽  
Vol 134 (7) ◽  
pp. 747-750 ◽  
Author(s):  
Rhian M. Touyz ◽  
Hongliang Li ◽  
Christian Delles

Abstract Angiotensin converting enzyme 2 (ACE2) is the major enzyme responsible for conversion of Ang II into Ang-(1-7). It also acts as the receptor for severe acute respiratory syndrome (SARS)-coronavirus (CoV)-2, which causes Coronavirus Disease (COVID)-19. In recognition of the importance of ACE2 and to celebrate 20 years since its discovery, the journal will publish a focused issue on the basic science and (patho)physiological role of this multifunctional protein.


Toxins ◽  
2020 ◽  
Vol 12 (12) ◽  
pp. 742
Author(s):  
Bogusz Trojanowicz ◽  
Christof Ulrich ◽  
Matthias Girndt

Apelin peptides (APLN) serve as second substrates for angiotensin-converting enzyme 2 (ACE2) and, in contrast to angiotensin II (AngII), exert blood-pressure lowering and vasodilatation effects through binding to G-coupled APLN receptor (APLNR). ACE2-mediated cleavage of the APLN may reduce its vasodilatory effects, but decreased ACE2 may potentiate the hypotensive properties of APLN. The role of APLN in uremia is unclear. We investigated the correlations between serum-APLN, leucocytic APLNR, and ACE2 in 32 healthy controls (NP), 66 HD, and 24 CKD3–5 patients, and the impact of APLN peptides on monocytic behavior and ACE2 expression under uremic conditions in vitro. We observed that serum APLN and leucocytic APLNR or SLCO2B1 were significantly elevated in uremic patients and correlated with decreased ACE2 on uremic leucocytes. APLN-treated THP-1 monocytes revealed significantly increased APLNR and ACE2, and reduced TNFa, IL-6, and MCSF. Uremic toxins induced a dramatic increase of miR-421 followed by significant reduction of ACE2 transcripts, partially counteracted with APLN-13 and -36. APLN-36 triggered the most potent transmigration and reduction of endothelial adhesion. These results suggest that although APLN peptides may partly protect against the decay of monocytic ACE2 transcripts, uremic milieu is the most dominant modulator of local ACE2, and likely to contribute to the progression of atherosclerosis.


2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Nisha Sharma ◽  
Anil Bhanudas Gaikwad

Abstract Background and Aims In clinical settings, diabetics remain on higher risk of ischemic renal injury (IRI) than nondiabetic patients. In addition, IRI predisposes distant organs to dysfunction such as neurological impairments via activation of the pressor arm of renin-angiotensin system (RAS). In contrast, the role of depressor arm of RAS on IRI-associated neurological sequalae remains elusive. Hence, this study explored the role of angiotensin II type 2 receptor (AT2R) and angiotensin-converting enzyme 2 (ACE2) in IRI-associated neurological dysfunctions under nondiabetic (ND) and diabetes mellitus (DM) condition. Method Type 1 diabetes was induced by injecting streptozotocin (55 mg/kg i.p.). ND and DM rats with bilateral IRI were treated with AT2R agonist-Compound 21 (C21) (0.3 mg/kg/day, i.p.) or ACE2 activator-Diminazene Aceturate (Dize), (5 mg/kg/day, p.o.) per se or in combination therapy. Behavioural, biochemical, and histopathological analysis were done to assess IRI-induced neurological impairment. Moreover, immunohistochemistry, ELISA and qRT-PCR experiments were conducted for molecular mechanism analysis. Result In ND and DM rats, IRI caused hippocampal complications as evidenced by increased MDA and nitrite levels, augmented inflammatory cytokines (granulocyte colony stimulating factor, glial fibrillary acidic protein), altered protein and mRNA expressions of Ang II, Ang-(1-7), AT1R, AT2R and MasR. In contrast, concomitant therapy of C21 and Dize effectively normalised aforementioned hippocampal alterations. The protective effect of combination therapy was exerted due to augmented protein and mRNA levels of depressor arm components. Conclusion The current study demonstrated the protective role of AT2R agonist and ACE2 activator in IRI-associated neurological dysfunction through preventing oxidative stress, inflammation and upregulating brain depressor arm of RAS under ND and DM conditions.


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