Drug Discovery Today

2019

DOI: 10.1016/j.drudis.2019.04.007

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Harnessing nucleic acid-based therapeutics for atherosclerotic cardiovascular disease: state of the art

Fatemeh Vahdat Lasemi

¹

,

Maryam Mahjoubin‐Tehran

²

,

Seyed Hamid Aghaee‐Bakhtiari

³

et al.

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Conventional and Novel Treatments2

Therapeutic Approaches For Atherosclerosis1

Angptl3‐targeted Therapies In Ascvd1

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Cited by 21 publications

(12 citation statements)

References 126 publications

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“…In addition to protein-based therapeutics (recombinant proteins and antibodies), efforts have been made toward the development of nucleic acid-based drugs which are stable and have longer half-lives than protein-based therapeutics [ 24 , 25 ]. The nucleic acid-based therapeutic approach includes antisense oligonucleotides (ASO), small interfering RNAs (siRNA), MicroRNAs (miRNA), and decoys [ 26 ].…”

Section: Therapeutic Approaches For Atherosclerosismentioning

confidence: 99%

Decoy Technology as a Promising Therapeutic Tool for Atherosclerosis

Mahjoubin‐Tehran

¹

,

²

,

³

et al. 2021

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Cardiovascular diseases (CVDs) have been classified into several types of disease, of which atherosclerosis is the most prevalent. Atherosclerosis is characterized as an inflammatory chronic disease which is caused by the formation of lesions in the arterial wall. Subsequently, lesion progression and disruption ultimately lead to heart disease and stroke. The development of atherosclerosis is the underlying cause of approximately 50% of all deaths in westernized societies. Countless studies have aimed to improve therapeutic approaches for atherosclerosis treatment; however, it remains high on the global list of challenges toward healthy and long lives. Some patients with familial hypercholesterolemia could not get intended LDL-C goals even with high doses of traditional therapies such as statins, with many of them being unable to tolerate statins because of the harsh side effects. Furthermore, even in patients achieving target LDL-C levels, the residual risk of traditional therapies is still significant thus highlighting the necessity of ongoing research for more effective therapeutic approaches with minimal side effects. Decoy-based drug candidates represent an opportunity to inhibit regulatory pathways that promote atherosclerosis. In this review, the potential roles of decoys in the treatment of atherosclerosis were described based on the in vitro and in vivo findings.

“…In addition to protein-based therapeutics (recombinant proteins and antibodies), efforts have been made toward the development of nucleic acid-based drugs which are stable and have longer half-lives than protein-based therapeutics [ 24 , 25 ]. The nucleic acid-based therapeutic approach includes antisense oligonucleotides (ASO), small interfering RNAs (siRNA), MicroRNAs (miRNA), and decoys [ 26 ].…”

Section: Therapeutic Approaches For Atherosclerosismentioning

confidence: 99%

Decoy Technology as a Promising Therapeutic Tool for Atherosclerosis

Mahjoubin‐Tehran

¹

,

²

,

³

et al. 2021

Self Cite

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Cardiovascular diseases (CVDs) have been classified into several types of disease, of which atherosclerosis is the most prevalent. Atherosclerosis is characterized as an inflammatory chronic disease which is caused by the formation of lesions in the arterial wall. Subsequently, lesion progression and disruption ultimately lead to heart disease and stroke. The development of atherosclerosis is the underlying cause of approximately 50% of all deaths in westernized societies. Countless studies have aimed to improve therapeutic approaches for atherosclerosis treatment; however, it remains high on the global list of challenges toward healthy and long lives. Some patients with familial hypercholesterolemia could not get intended LDL-C goals even with high doses of traditional therapies such as statins, with many of them being unable to tolerate statins because of the harsh side effects. Furthermore, even in patients achieving target LDL-C levels, the residual risk of traditional therapies is still significant thus highlighting the necessity of ongoing research for more effective therapeutic approaches with minimal side effects. Decoy-based drug candidates represent an opportunity to inhibit regulatory pathways that promote atherosclerosis. In this review, the potential roles of decoys in the treatment of atherosclerosis were described based on the in vitro and in vivo findings.

“…Antisense oligonucleotides (ASO) are synthetic single‐stranded nucleic acid oligonucleotides, which can promote targeting mRNA degradation, or interdict their translation or splicing through binding to the complementary mRNA species 100 . Multiple ASO are currently being developed against ASCVD 101 …”

Section: Angptl3‐targeted Therapies In Ascvdmentioning

confidence: 99%

Targeting angiopoietin‐like 3 in atherosclerosis: From bench to bedside

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²

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³

et al. 2021

Diabetes Obesity Metabolism

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Atherosclerotic cardiovascular disease (ASCVD) is the largest cause of morbidity and mortality worldwide. Lipid‐lowering therapies are the current major cornerstone of ASCVD management. Statins, ezetimibe, fibrates and proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors effectively reduce the plasma low‐density lipoprotein cholesterol (LDL‐C) level in most individuals at risk of atherosclerosis. Still, some patients (such as those with homozygous familial hypercholesterolaemia), who do not respond to standard therapies, and other patients who cannot take these agents, remain at a high risk of ASCVD. In recent years there has been tremendous progress in understanding the mechanism and efficacy of lipid‐lowering strategies. Apart from the recently approved PCSK9 and ATP citrate lyase inhibitors, angiopoietin‐like 3 (ANGPTL3) is another potential target for the treatment of dyslipidaemia and its clinical sequalae of atherosclerosis. ANGPTL3 is a pivotal modulator of plasma triglycerides (TG), LDL‐C and high‐density lipoprotein cholesterol (HDL‐C) levels, achieved by inhibiting the activities of lipoprotein lipase and endothelial lipase. Familial combined hypolipidaemia is derived from the Angptl3 loss‐of‐function mutations, which leads to low levels of LDL‐C, HDL‐C and TG, and has a 34% decreased risk of ASCVD compared with non‐carriers. To date, monoclonal antibodies (evinacumab) and antisense oligonucleotides against ANGPTL3 have been investigated in clinical trials for dyslipidaemia therapy. Herein, we review the biology and function of ANGPTL3, as well as the latest developments of ANGPTL3‐targeted therapies. We also summarize evidence from basic research to clinical trials, with the aim of providing novel insights into the biological functions of ANGPTL3 and related targeted therapies.

“…Arca et al provided evidence showing that atorvastatin (average dose of 20 mg/d) is superior to fenofibrate (200 mg/d) in treating hyperlipidemia in FCHL patients . There are also several novel therapies for the management of hypertriglyceridemia that might find applications in future, either alone or in combination with other agents, for the management of FCHL .…”

Section: Conventional and Novel Treatmentsmentioning

confidence: 99%

“…Despite various studies about the superiority of combination therapy, some researchers have recently tried to establish (89). There are also several novel therapies for the management of hypertriglyceridemia that might find applications in future, either alone or in combination with other agents, for the management of FCHL (90,91). While statins can lower plasma cholesterol and fibrates can lower both plasma cholesterol and TGs, there is a need for drugs, which can improve LDL phenotype as well (92).…”

Section: Conventional and Novel Treatmentsmentioning

confidence: 99%

Familial combined hyperlipidemia: An overview of the underlying molecular mechanisms and therapeutic strategies

¹

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²

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³

et al. 2019

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Among different types of dyslipidemia, familial combined hyperlipidemia (FCHL) is the most common genetic disorder, which is characterized by at least two different forms of lipid abnormalities: hypercholesterolemia and hypertriglyceridemia. FCHL is an important cause of cardiovascular diseases. FCHL is a heterogeneous condition linked with some metabolic defects that are closely associated with FCHL. These metabolic features include dysfunctional adipose tissue, delayed clearance of triglyceride‐rich lipoproteins, overproduction of very low‐density lipoprotein and hepatic lipids, and defect in the clearance of low‐density lipoprotein particles. There are also some genes associated with FCHL such as those affecting the metabolism and clearance of plasma lipoprotein particles. Due to the high prevalence of FCHL especially in cardiovascular patients, targeted treatment is ideal but this necessitates identification of the genetic background of patients. This review describes the metabolic pathways and associated genes that are implicated in FCHL pathogenesis. We also review existing and novel treatment options for FCHL. © 2019 IUBMB Life, 71(9):1221–1229, 2019

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