The role and significance of angiotensin‐converting enzyme 2 peptides in the treatment of coronavirus disease 2019

Abstract

At the end of December 2019, a newly discovered coronavirus (severe acute respiratory syndrome coronavirus 2 [SARS-CoV-2]) rapidly swept across China. The virus causes coronavirus disease 2019 (COVID-19), leading to severe sequelae, such as acute respiratory distress, septic shock, and multiple organ dysfunction/failure. [1][2][3] Thus, COVID-19 poses a serious threat to human life. Since March 2020, the novel coronavirus has spread rapidly worldwide. By March 2021, there have been more than 117.6 million confirmed cases and 2.6 million deaths worldwide, with a mortality rate of >2%. Despite the measures taken worldwide, the virus continues to spread, and the duration of the pandemic remains unknown.In early case reports, SARS-CoV-2 was considered to be less severe than the SARS-CoV and Middle East respiratory syndrome coronavirus (MERS-CoV) that caused outbreaks in 2003 and 2012, respectively. [4][5][6] However, based on the extensive transmission of the virus and the rapid progression of the disease, increasing evidence shows that SARS-CoV-2 is more infectious and harmful, 7 and its impact on human health and the world economy is far greater than that of SARS-CoV and MERS-CoV. In the face of the sudden disaster, scientists worldwide strive to develop vaccines and specific drugs for the treatment of this disease. Thus far, several vaccines against COVID-19 have been approved and utilized. Despite the occurrence of some adverse events, the effectiveness of the vaccines has been affirmed. However, investigators have not yet discovered

The potential role of synovial cells in the progression and treatment of osteoarthritis

“…[79] A similar study demonstrated that co-culture of SMSCs with chondrocytes down-regulated the expression of MMP-13 and up-regulated the expression of COL2A1, Aggrecan, while injection of SMSCs into the joints of OA rats suppressed the secretion of inflammatory factors and increased the expression of COL2A1, Aggrecan. [80] In addition, EVs secreted by MSCs represent another paracrine mechanism which plays an important role in reducing inflammation and cartilage damage (Figure 2). EVs from MSCs contain many bioactive components, such as microR-NAs and proteins, which are transferred to target cells via the paracrine pathway, providing an immunosuppressive effect.…”

“…[ 79 ] A similar study demonstrated that co‐culture of SMSCs with chondrocytes down‐regulated the expression of MMP‐13 and up‐regulated the expression of COL2A1, Aggrecan, while injection of SMSCs into the joints of OA rats suppressed the secretion of inflammatory factors and increased the expression of COL2A1, Aggrecan. [ 80 ]…”

Severe Acute Respiratory Syndrome Coronavirus 2 Receptor (Human Angiotensin-Converting Enzyme 2) Binding Inhibition Assay: A Rapid, High-Throughput Assay Useful for Vaccine Immunogenicity Evaluation

“…SARS-CoV-2 infects cells by binding of viral S-protein to the receptor, human angiotensin-converting enzyme 2 (hACE2), on the target cell [ 10 ]. Results of several studies have demonstrated that blocking this binding process can prevent infection by SARS-CoV-2 [ 11 , 12 , 13 , 14 ], and hACE2 binding is widely thought to be a promising target for future COVID-19 therapeutics [ 15 , 16 ]. This article describes the development of an in vitro assay to detect inhibition of S-protein binding to hACE2 (most likely by anti-S antibodies) for the ancestral strain of SARS-CoV-2 and the Delta and Omicron BA.1/BA.5 variants.…”

ACE2, a drug target for COVID-19 treatment?

“…In a previous article reported by our research group, the essential role of soluble ACE2 or ACE2-specific small molecular peptides targeting ACE2 in preventing the virus from entering the human body was summarized, thereby suggesting ACE2 as the potential target for the development of specific drugs against the COVID-19 virus [13]. Although it is feared that both Alpha (the earlier variant) and Omicron (the current variant) variants may mutate and become capable of escaping the immunity elicited by antibodies, the virus would continue to have a binding affinity for ACE2, and the binding force between the virus and ACE2 is expected to become stronger with each mutation [14,15].…”