The first cases of patients infected with SARS-Cov-2 virus were recorded in China in November 2019, and then rapidly spread to all countries around the world, causing a global pandemic. Much is known about the pathophysiology of this virus infection, but perhaps not enough. One of the aspects still to be investigated is the correlation between the renin-angiotensin system (RAS) and SARS-Cov-2 infection. RAS is a physiological system with a key role in regulating the different functions of the human body. SARS-CoV-2, uses the enzyme ACE-2 as a potential factor of cell penetration and infectivity, moreover in the different stages of infection a functional variation of the RAS system has been noted in different targets and at different times. In particular, in this article, we discuss the role of RAS on SARS-Cov-2 infection, and possible therapies that acting modifiers the system.

An acute respiratory disease, caused by a novel coronavirus (SARS-CoV-2) has spread throughout China and other countries and received worldwide attention. On 30 January 2020, World Health Organization (WHO) officially declared the SARS-CoV-2 epidemic as a public health emergency of international concern. At the moment of writing this article (April 2020) a total of 2.240.191 cases confirmed worldwide since the outbreak and 153.822 deaths in 166 countries or regions confirmed cases globally had been reported. Meanwhile, several independent research groups have identified that SARS-CoV-2 has highly identical genome with SARS-COV-1. The novel coronavirus uses the same receptor, angiotensin-converting enzyme 2 (ACE2) as that for SARS-CoV, and mainly spreads through the respiratory tract. The clinical symptoms of patients include fever, cough, fatigue and a small population of patients appeared gastrointestinal infection symptoms. Currently, there are few specific therapeutic strategies, but several potent candidates of antivirals and repurposed drugs are under urgent investigation. In this review, we summarized the current treatment and scientific advancements to combat the epidemic novel coronavirus. Keywords: SARS-CoV-2, treatment, coronavirus, infection, pneumonia

For some patients with SARS-CoV-2, the worst clinical damage is not caused by the virus itself, but by an overactive inflammatory state. In fact, in some people the immune system goes into overdrive and launches a large-scale assault on the tissue known as cytokine storm. This excessive immune reaction can damage tissue and eventually kill people. Several tests show that blocking such cytokine storms can be effective, studies are underway to test drugs that act by reducing cytokine response, such as tocilizumab and sarilumab that bind interleukin 6 (IL-6) or anikinra which is the interleukin 1 receptor antagonist (IL-1). However, other drugs that block the cytokine cascade can also be considered. In this article we describe the scientific and molecular motivation for the use of drugs that act by modulating the inflammatory system in patients with SARS-CoV-2, considering in particular an old drug that has been in use for many years for other therapeutic indications such as colchicine, and that could be favorable its use to block the cytokine cascade in SARS-CoV-2 patients, with low cost and good tolerability.

About 300 million people worldwide are affected by rheumatic diseases and over 5 and a half million men and women affected by rheumatological diseases are present in Italy. These are chronic diseases and therefore require treatment and diagnostic tests for long periods of time. Patient needs must be met even in these difficult months marked by the COVID-19 pandemic. The guarantee of therapeutic continuity is important and increasingly dangerous is the lack of many drugs. This is because many antimalarial and anti-inflammatory drugs have entered the protocols for treatment from Sars Cov 2. Without taking these medicines, which for years have also been used in rheumatology, there is a risk of reactivating serious diseases including rheumatoid arthritis, ankylosing spondylitis or systemic Lupus erythematosus.

For some patients with SARS-CoV-2, the worst clinical damage is not caused by the virus itself, but by an overactive inflammatory state. In fact, in some people the immune system goes into overdrive and launches a large-scale assault on the tissue known as cytokine storm. This excessive immune reaction can damage tissue and eventually kill people. Evidence shows that blocking such cytokine storms can be effective, so trials are underway to test drugs that act by reducing the cytokine response, such as tocilizumab and sarilumab that bind interleukin 6 (IL-6), or anikinra that is interleukin 1 (IL-1) receptor antagonist. However, other drugs that block the cytokine cascade may also be considered. In this article we describe the scientific and molecular motivation for the use of drugs that act by modulating the inflammatory system in patients affected by SARS-CoV-2, considering in particular an old drug that has been in use for many years for other therapeutic indications such as colchicine, and that could result favorable its use, with low cost and good tolerability.

Several studies have shown a high correlation between concentration and development of low-density lipoprotein cholesterol (LDL-C)and the evolution of atherosclerosis and cardiovascular disease. Therefore, the reduction of LDL-C levels through lifestyle modification and/or pharmacological interventions has universally shown a decrease in cardiovascular events and mortality. In most cases, elevated blood lipid levels may be caused by alterations in certain genes encoding proteins involved in LDL metabolism, such as those associated with loss of function of the LDLr receptor gene , loss of function of the apoB gene or increased function of a PCSK9 protein .Family hypercholesterolemia is a hereditary disease in which a genetic alteration causes an increase in blood cholesterol. Therapy is based on dietary control and drugs such as statins, ezetimibe or PCSK9 inhibitory monoclonal antibodies. An important scientific breakthrough in recent years is the ability to identify the genetic basis of diseases and possibly correct the defective gene by interfering with small interfering RNA (siRNA) or antisense oligonucleotides (ASO). The technologies of antisense oligonucleotides (ASOs) and small interfering RNAs (siRNAs) have also been developed for the treatment of hypercholesterolemia with the aim of controlling the expression of specific genes that play key roles in lipid metabolism. Anti-sense oligonucleotides have been developed to target apolipoprotein B, the main structural protein of VLDL,LDL and chylomicrons,apolipoproteinCIII or angiopoietin 3, both of which play a role in the regulation of triglyceridesorapo(a). The siRNA approach works on the expression of PCSK9, a key modulator in LDL receptor catabolism. The purpose of this review is to present and discuss current clinical and scientific data on therapeutic evidence for new gene therapies in the treatment of hypercholesterolemia.

Glyphozines also called SGLT2 inhibitors, are a new class of agents that inhibit reabsorption of glucose in the kidney, in proxinal tubules, and therefore lower blood sugar. They act by inhibiting sodium-glucose transport protein 2 (SGLT2). Glyphozines are used in the treatment of type II diabetes mellitus (T2DM). In studies with canagliflozin, a member of this class, the medication was found to enhance blood sugar control as well as reduce body weight and systolic and diastolic blood pressure.[1] In addition to regulate blood glucose, recent studies have shown that glyphozines have important positive cardiovascular benefits, such as weight loss, decreased volaemia and PA, reduced triglycerides, natriuresis and improved endothelial wall dysfunction. Clinical studies have shown reduction in deaths from cardiovascular events among diabetic patients treated with glyphozines. At the moment these drugs are being studied for an extension of the therapeutic indication also for cardiovascular diseases such as heart failure. In this review, we discuss the class of SGLT2 inhibitors in the treatment of diabetes, and studies focused on their possible role in the treatment of cardiac disease.

In recent years, new classes of drugs have entered the market for the treatment of type 2 diabetes mellitus (T2DM) with good efficacy on the normalization of blood glucoseandwithareductionin the risk of hypoglycaemia and with significant effects on weight reduction. One of the most promising classes in achieving these goals was that of the agonists(GLP)-1.However,adifficulty in using these drugs arisesfromsubcutaneousadministration,aroutethatisnotveryconvenientfor users and with the risk of infections. More recently, a GLP-1 agonist, semaglutide, has been developedwhichcanbeadministeredorally.Inthisreviewarticle,wediscussedtheeffectivenessof GLP-1 agonists, oral semaglutide and its therapeutic potential.