Basic Pathogenic Mechanisms and Epigenetic Players Promoted by Extracellular Vesicles in Vascular Damage

Schiano, Concetta; Balbi, Carolina; Nigris, Filomena de; Napoli, Claudio

doi:10.3390/ijms24087509

Cited by 4 publications

(3 citation statements)

References 157 publications

(206 reference statements)

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“…Indeed, depending on the specific cell source, EVs hold great potential for use in the diagnosis and prognosis of cardiac dysfunction, as well as novel therapeutic agents, particularly in the context of acute myocardial infarction and heart failure [ 43 , 44 ]. Their role as diagnostic elements, providing insight into disease onset and the contribution of the different cardiac cells to pathophysiological progression, has been recently demonstrated in different studies [ 45 , 46 , 47 , 48 , 49 ]. Since EVs may play a key role in the myocardial immune response and inflammation, they have been suggested as non-invasive biomarkers for CVD.…”

Section: Exploiting Evs In Cardiovascular Diseasementioning

confidence: 99%

Evolving Strategies for Extracellular Vesicles as Future Cardiac Therapeutics: From Macro- to Nano-Applications

Guerricchio,

Barile,

Bollini

2024

IJMS

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Cardiovascular disease represents the foremost cause of mortality and morbidity worldwide, with a steadily increasing incidence due to the growth of the ageing population. Cardiac dysfunction leading to heart failure may arise from acute myocardial infarction (MI) as well as inflammatory- and cancer-related chronic cardiomyopathy. Despite pharmacological progress, effective cardiac repair represents an unmet clinical need, with heart transplantation being the only option for end-stage heart failure. The functional profiling of the biological activity of extracellular vesicles (EVs) has recently attracted increasing interest in the field of translational research for cardiac regenerative medicine. The cardioprotective and cardioactive potential of human progenitor stem/cell-derived EVs has been reported in several preclinical studies, and EVs have been suggested as promising paracrine therapy candidates for future clinical translation. Nevertheless, some compelling aspects must be properly addressed, including optimizing delivery strategies to meet patient needs and enhancing targeting specificity to the cardiac tissue. Therefore, in this review, we will discuss the most relevant aspects of the therapeutic potential of EVs released by human progenitors for cardiovascular disease, with a specific focus on the strategies that have been recently implemented to improve myocardial targeting and administration routes.

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Section: Exploiting Evs In Cardiovascular Diseasementioning

confidence: 99%

Evolving Strategies for Extracellular Vesicles as Future Cardiac Therapeutics: From Macro- to Nano-Applications

Guerricchio,

Barile,

Bollini

2024

IJMS

View full text Add to dashboard Cite

show abstract

“…This process occurs due to inflammation, the oxidation of LDL particles, endothelial dysfunction, foam cell formation, proliferation, and the migration of vascular smooth muscle cells (VSMCs) [ 29 ]. The preceding vascular modifications are also affected by extracellular matrix molecules, soluble factors, and interactions between endothelial cells (EC) and EVs [ 30 ]. EVs are associated with critical steps in atherosclerosis, cholesterol metabolism, immune response endothelial dysfunction, and vascular inflammation and remodeling [ 31 , 32 ].…”

Section: Evs In Atherosclerosis and Cardiovascular Diseasesmentioning

confidence: 99%

Extracellular Vesicles in Atherosclerosis: State of the Art

Olejarz,

Sadowski,

Radoszkiewicz

2023

IJMS

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Atherosclerosis is a chronic inflammatory disease driven by lipid accumulation in the arteries, leading to narrowing and thrombosis that causes mortality. Emerging evidence has confirmed that atherosclerosis affects younger people and is involved in the majority of deaths worldwide. EVs are associated with critical steps in atherosclerosis, cholesterol metabolism, immune response, endothelial dysfunction, vascular inflammation, and remodeling. Endothelial cell-derived EVs can interact with platelets and monocytes, thereby influencing endothelial dysfunction, atherosclerotic plaque destabilization, and the formation of thrombus. EVs are potential diagnostic and prognostic biomarkers in atherosclerosis (AS) and cardiovascular disease (CVD). Importantly, EVs derived from stem/progenitor cells are essential mediators of cardiogenesis and cardioprotection and may be used in regenerative medicine and tissue engineering.

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“…Cardiovascular disease (CVD) is one of the leading causes of death worldwide [ 1 ]. The formation of atherosclerotic plaques obstructs blood flow to organs, the clinical manifestations of which include myocardial infarction (MI), ischemic heart disease (IHD), and stroke, which are the main causes of CVD [ 2 – 5 ].…”

Section: Introductionmentioning

confidence: 99%

The translational potential of miR-26 in atherosclerosis and development of agents for its target genes ACC1/2, COL1A1, CPT1A, FBP1, DGAT2, and SMAD7

Chen,

Wu,

et al. 2024

Cardiovasc Diabetol

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Atherosclerosis is one of the leading causes of death worldwide. miR-26 is a potential biomarker of atherosclerosis. Standardized diagnostic tests for miR-26 (MIR26-DX) have been developed, but the fastest progress has been in predicting the efficacy of IFN-α therapy for hepatocellular carcinoma (HCC, phase 3). MiR-26 slows atherosclerosis development by suppressing ACC1/2, ACLY, ACSL3/4, ALDH3A2, ALPL, BMP2, CD36, COL1A1, CPT1A, CTGF, DGAT2, EHHADH, FAS, FBP1, GATA4, GSK3β, G6PC, Gys2, HMGA1, HMGB1, LDLR, LIPC, IL-1β, IL-6, JAG2, KCNJ2, MALT1, β-MHC, NF-κB, PCK1, PLCβ1, PYGL, RUNX2, SCD1, SMAD1/4/5/7, SREBF1, TAB3, TAK1, TCF7L2, and TNF-α expression. Many agents targeting these genes, such as the ACC1/2 inhibitors GS-0976, PF-05221304, and MK-4074; the DGAT2 inhibitors IONIS-DGAT2Rx, PF-06427878, PF-0685571, and PF-07202954; the COL1A1 inhibitor HT-100; the stimulants 68Ga-CBP8 and RCT-01; the CPT1A inhibitors etomoxir, perhexiline, and teglicar; the FBP1 inhibitors CS-917 and MB07803; and the SMAD7 inhibitor mongersen, have been investigated in clinical trials. Interestingly, miR-26 better reduced intima-media thickness (IMT) than PCSK9 or CT-1 knockout. Many PCSK9 inhibitors, including alirocumab, evolocumab, inclisiran, AZD8233, Civi-007, MK-0616, and LIB003, have been investigated in clinical trials. Recombinant CT-1 was also investigated in clinical trials. Therefore, miR-26 is a promising target for agent development. miR-26 promotes foam cell formation by reducing ABCA1 and ARL4C expression. Multiple materials can be used to deliver miR-26, but it is unclear which material is most suitable for mass production and clinical applications. This review focuses on the potential use of miR-26 in treating atherosclerosis to support the development of agents targeting it.

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Basic Pathogenic Mechanisms and Epigenetic Players Promoted by Extracellular Vesicles in Vascular Damage

Cited by 4 publications

References 157 publications

Evolving Strategies for Extracellular Vesicles as Future Cardiac Therapeutics: From Macro- to Nano-Applications

Evolving Strategies for Extracellular Vesicles as Future Cardiac Therapeutics: From Macro- to Nano-Applications

Extracellular Vesicles in Atherosclerosis: State of the Art

The translational potential of miR-26 in atherosclerosis and development of agents for its target genes ACC1/2, COL1A1, CPT1A, FBP1, DGAT2, and SMAD7

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