CRISPR‑Cas9: A New Frontier in the Treatment and Research of

Cardiovascular Diseases

Jinnan Jiao

Xi'an Qujiang Kangchiao School, Xi'an, China

Keywords: CRISPR‑Cas9, Cardiovascular Diseases, Gene Therapy.

Abstract: CRISPR-Cas9 provides accurate and effective techniques for altering genetic sequences, revolutionizing the

field of genome editing, which holds significant potential for treating cardiovascular diseases (CVD) by

correcting pathogenic mutations and modulating gene expression. LDLR gene mutations have been

successfully corrected using CRISPR-Cas9, which is associated with familial hypercholesterolemia, thereby

improving the atherosclerotic phenotype in mouse models. Additionally, CRISPR-Cas9 shows promise in

treating familial cardiomyopathies by correcting mutations in genes such as RBM20 and MYH6, leading to

the restoration of normal cardiac function. However, several challenges remain, including off-target effects,

which leads to unintended genetic alterations, and delivery challenges that limit the precise targeting of

cardiovascular tissues. The creation of innovative delivery systems, like lipid nanoparticles, is one area of

future research, to enhance specificity and reduce off-target effects. Personalized medicine may benefit from

the combination of CRISPR-Cas9 and next-generation sequencing, which could result in the development of

CVD cures.

1 INTRODUCTION

Cardiovascular disease (CVD) continues to represent

the majority of morbidity and mortality worldwide.

The World Health Organization estimates that around

17.9 million people died globally in 2019，due to

cardiovascular issues. These deaths accounted for

32% of the total fatalities, which places a significant

financial burden on healthcare systems (Amini et al.

2021). The pathophysiology of cardiovascular

disease is complex, involving multiple genetic and

environmental factors, and developing effective

prevention and treatment strategies is bound to be a

daunting challenge (Cheng et al. 2024). In recent

years, the introduction of CRISPR-Cas9 technology

(Clustered Regularly Interspaced Short Palindromic

Repeats) has brought about a major transformation in

molecular biology. The bacterial adaptive immune

system is the source of both CRISPR and the protein

Cas9. This system enables bacteria to recognize

foreign and cut DNA, such as DNA from invading

viruses. In the lab, researchers use this natural defense

mechanism for precise gene editing. A Cas9 nuclease

that cuts DNA at the target location and a single

conducting RNA that detects a particular DNA

sequence make up the CRISPR-Cas9 mechanism.

Once the DNA has been sliced, desired genetic

alterations, such as gene knockouts, knockins, or

point mutations, can be introduced by utilizing the

cell's natural DNA repair systems. The possibilities of

CRISPR-Cas9 technology within cardiovascular

disease is enormous. Because many cardiovascular

diseases have a genetic basis, the ability to precisely

edit genes offers additional avenues for

understanding disease mechanisms and developing

new therapies.

Several studies have demonstrated the promise

of CRISPR-Cas9 in cardiovascular research

(Bharucha et al. 2022). In animal models, the

researchers have successfully used CRISPR-Cas9

to modify genes involved in lipid metabolism,

which is crucial in the development of

atherosclerosis. By knocking out genes involved in

cholesterol synthesis or uptake, it has been possible

to reduce plaque formation in the arteries. In

addition, in heart failure models, CRISPR-Cas9 has

been used to manipulate genes involved in heart

remodeling, showing potential to improve heart

function. Despite these exciting advances, many

challenges remain. The main problem is the off-

target effect. The CRISPR-Cas9 system may cut

362

Jiao, J.

CRISPR-Cas9: A New Frontier in the Treatment and Research of Cardiovascular Diseases.

DOI: 10.5220/0014493400004933

Paper published under CC license (CC BY-NC-ND 4.0)

In Proceedings of the 1st International Conference on Biomedical Engineering and Food Science (BEFS 2025), pages 362-367

ISBN: 978-989-758-789-4

DNA at locations other than the intended target,

leading to unintended genetic changes that could be

harmful. Another challenge is effectively delivering

CRISPR-Cas9 components to target cells in the

cardiovascular system. The heart and blood vessels

are complex organs, which requires ensuring that

the gene-editing mechanism reaches the appropriate

cells without causing damage to the surrounding

tissues (Bonowicz et al. 2025). This review

provided a thorough summary of the state of the use

of CRISPR-Cas9 in cardiovascular disease research

and treatment. In this quickly developing topic, the

most recent research developments, difficulties, and

possible future paths were examined. The creation

of safer and more efficient gene-based therapies for

cardiovascular disease is facilitated by an

awareness of the state of the technology today. the

creation of safer and more efficient gene-based

treatments for heart conditions.

2 AN OVERVIEW OF CRISPR-

Cas9 TECHNOLOGY

2.1 Mechanisms of CRISPR-Cas9

Technology

As a groundbreaking technology in molecular

biology, the CRISPR-Cas9 gene-editing system is

engineered based on the natural immune defense

mechanisms of bacteria. This system comprises two

core functional modules: (1) Cas9 Nuclease:

Functions as "molecular scissors" for site-specific

double-strand DNA cleavage. (2) Single-Guide RNA

(sgRNA): Serves as a navigation system that enables

precise genomic targeting through base

complementary pairing. The mechanism of action

follows a refined three-stage workflow: (1) Target

Recognition: sgRNA binds specifically to the target

DNA sequence. (2) Nuclease Activation: Cas9

protein executes precise DNA cleavage at

predetermined genomic coordinates. (3) Genetic

Reprogramming: Cellular autonomous repair

mechanisms (primarily via non-homologous end

joining [NHEJ] or homology-directed repair [HDR]

pathways) mediate genomic modifications,

ultimately achieving precise edits including gene

inactivation, sequence insertion, and single-base

substitutions.

The CRISPR-Cas9 system demonstrates

remarkable utility in functional genomics research.

In genome-wide functional screening applications,

this technology enables comprehensive analysis of

gene functions. Taking gene knockout as an

example, by specifically targeting and inactivating

genomic loci through coordinated delivery of large-

scale sgRNA libraries and Cas9 protein, researchers

can systematically identify key genes involved in

cellular processes and drug resistance mechanisms,

establishing a novel research paradigm for

elucidating genetic disease etiology (Shalem et al.

2015). Particularly noteworthy is the system's

capability for precise gene expression modulation.

By fusing transcriptional regulatory elements with

catalytically inactive dCas9 protein, researchers can

upregulate or downregulate target gene expression

without altering DNA sequences (Lee et al. 2024).

This innovative approach has pioneered new

avenues for gene function studies.

2.2 Advantages of CRISPR-Cas9

Technology

The CRISPR-Cas9 system's simplicity and efficiency

have positioned it as a preferred tool for genome

editing. CRISPR-Cas9 is easier to design and perform

when compared with older gene-editing technologies

such as zinc-finger nucleases (ZFNs) and

transcriptional activator-like effector nucleases

(TALENs) because it relies on RNA-DNA

interactions rather than intricate protein engineering.

This system can be easily reprogrammed by altering

the sgRNA sequence to target different genomic loci,

allowing for high-throughput and multiplexed gene

editing (Shojaei Baghini et al. 2022).

2.3 Applications of CRISPR-Cas9

Technology in High-Throughput

Functional Genomics

CRISPR-Cas9 has been instrumental in genome-scale

screening, enabling researchers to identify critical

genes for various cellular functions and responses. By

delivering Cas9 and sgRNA libraries into cells,

scientists can perform knockout screens to determine

gene essentiality and function. For instance, Shalem

et al. demonstrated the use of CRISPR-Cas9 for

genome-wide screens, identifying genes involved in

cellular viability and drug resistance (Shalem et al.

2015). This approach has been crucial for

understanding the genetic basis of diseases and

mechanisms of drug resistance.

CRISPR-Cas9: A New Frontier in the Treatment and Research of Cardiovascular Diseases

363

2.4 Transcriptional Modulations of

CRISPR-Cas9 Technology

In addition to gene deletion, CRISPR-Cas9 has the

ability to alter gene expression. By combining

transcriptional activator or repressor domains with

catalytically inactive Cas9 (dCas9), researchers can

precisely regulate gene expression without altering

the DNA sequence. Studying gene function and

creating treatment plans for illnesses where gene

control is involved have benefited greatly from this.

2.5 Challenges and Future Directions

of CRISPR-Cas9 Technology

CRISPR-Cas9 has several challenges despite the

many benefits it offers. Off-target effects, in which

unwanted parts of the genome are cleaved and may

result in dangerous mutations, are a major problem.

Researchers are creating methods to lessen this, like

refining sgRNA design and employing high-fidelity

Cas9 variations. Additionally, delivering the CRISPR

components efficiently and specifically to target cells

remains a hurdle, especially for in vivo applications.

Future research will focus on enhancing the

specificity and efficiency of CRISPR-Cas9, exploring

alternative Cas proteins, and developing novel

delivery systems. CRISPR-Cas9 has transformed the

landscape of molecular biology and holds immense

potential for advancing our understanding and

treatment of genetic diseases. Its applications in

genome editing, transcriptional regulation, and high-

throughput screening have already yielded significant

insights. As researchers continue to refine technology

and address its challenges, CRISPR-Cas9 is

positioned to play a pivotal role in the future of

genetic medicine.

3 THE USE OF CRISPR-Cas9 IN

THE TREATMENT OF

CARDIOVASCULAR DISEASES

3.1 Repairing Gene Mutations

Cardiovascular disease (CVD) has a genetic basis,

and CRISPR-Cas9 offers great potential for

correcting pathogenic mutations (Lloyd-Jones et al.

2006). LDLR gene mutations are the classic cause of

familial hypercholesterolemia (FH). In a mouse

model with the LdlrE208X mutation, Zhao et al.

showed that CRISPR-Cas9 delivered by AAV8

improved the atherosclerotic phenotype and largely

restored LDL receptor expression. Treated mice had

reduced cholesterol levels and smaller atherosclerotic

plaques. There is also hope that CRISPR-Cas9 can be

used to treat familial cardiomyopathies. In dilated

cardiomyopathy (DCM), the ABEmax-VRQR-

SpCas9 system was used to correct mutations in the

RBM20 gene in induced pluripotent stem cells

(iPSCs) and mouse heart tissue. As a result, the

dilatation of the heart was reversed, and the heart's

normal function was restored (Nammi et al. 2024).

For hypertrophic cardiomyopathy (HCM), AAV9-

targeted delivery of sgRNA to the MYH6 locus in

cardiomyocytes inactivated the pathogenic allele in

more than 70% of ventricular myocytes, preventing

the development of structural and functional features

of HCM in treated mice (Smolderen et al. 2024). In

addition to these applications, CRISPR-Cas9 has

been used to target other cardiovascular conditions.

For instance, Ding et al. showed that CRISPR-Cas9

could knock out the Pcsk9 gene in mice, leading to a

significant reduction in plasma cholesterol levels.

This approach has the potential to prevent

atherosclerosis and related cardiovascular diseases. In

a similar vein, Wang et al. showed that human

hepatocytes with mutations in the ApoB gene, linked

to familial hypercholesterolemia, could be corrected

using CRISPR-Cas9. These investigations

demonstrate the adaptability and promise of CRISPR-

Cas9 in the management of various cardiovascular

disorders.

Despite these promising results, several

challenges remain. Negative genetic changes may

result from off-target impacts, in which the CRISPR-

Cas9 mechanism cleaves DNA at unwanted locations.

High-fidelity Cas9 variants, such SpCas9-HF1, have

been created by researchers to solve this problem by

lowering off-target activity. Furthermore, the creation

of base editors has demonstrated promise in lowering

off-target effects. These editors combine nucleotide

deaminases and Cas9 nickases to accomplish single

nucleotide conversion without causing double-strand

breaks (DSBs). Delivering the components of

CRISPR-Cas9 to the intended tissues presents

another difficulty. Viral vectors, such as AAV, are

commonly used but can result in permanent

expression of nuclease proteins, leading to undesired

DNA cleavage. Non-viral delivery methods, such as

lipid nanoparticles and synthetic polymers, offer

alternatives that can reduce immunogenicity and

toxicity. For example, polysaccharide-based delivery

systems have shown potential in overcoming delivery

challenges while advancing the pharmaceutical

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applications of CRISPR-Cas9 gene therapy. By

repairing harmful mutations, CRISPR-Cas9

technology has enormous potential for treating

cardiovascular disorders. Realizing the full

therapeutic potential of CRISPR-Cas9 requires

ongoing research into enhancing its precision,

creating high-fidelity variations, and streamlining

delivery systems.

3.2 Regulating Protein Expression

CRISPR-Cas9 can cure cardiovascular illnesses by

modifying protein expression in addition to

correcting mutations. Targeting genes linked to

protein overexpression has showed potential in

hypertension. For instance, in adult rats with

spontaneous hypertension, systolic and diastolic

blood pressure were considerably lowered when exon

2 of the angiotensinogen (AGT) gene was disrupted

in hepatocytes using AAV8-Cas9-AGT gRNA.

Partial suppression of AGT expression was adequate

to avoid hypertension without altering cardiovascular

stress responses (Okobi et al. 2024). In

atherosclerosis, overexpression of proteins such as

APOC3 and PCSK9 contributes to disease

progression. When CRISPR-Cas9 disrupted APOC3

exon 2 in rabbits and hamsters, plasma triglycerides

decreased, HDL-C levels rose, and aortic plaque

formation decreased (Morgan et al. 2024). In a mouse

model, CRISPR-Cas9 genome editing of the Pcsk9

gene effectively reduced plasma cholesterol levels by

disrupting the gene, showing its potential to improve

cholesterol metabolism and reduce the risk of

cardiovascular disease (Shalem et al. 2015).

3.3 Targeting Mitochondrial

Dysfunction

Mitochondrial dysfunction is an important cause of

CVD. Mitochondrial DNA (mtDNA) mutations

impair energy metabolism and lead to diseases such

as hypertrophic cardiomyopathy, ischemic heart

disease, and heart failure. Sukhorukov et al. used

hybrid cell lines to study the m.15059G > A mutation

in the MT-CYB gene. This mutation disrupts

mitophagy and results in a persistent inflammatory

state. The researchers were able to eradicate the

mutated mtDNA copies, restore mitophagy, and

lower proinflammatory reactions by using CRISPR-

Cas9-based mitochondrial genome editing. However,

due to the bilayer mitochondrial membrane, it is still

difficult to deliver gRNA to the mitochondria.

Enhancing mitochondrial import through gRNA

modification with mitochondrial localization signals

(MLS) or the addition of stem-loop motifs is the aim

of current research, but more work is needed to

develop reliable delivery mechanisms (Yang et al.

2023).

4 CHALLENGES OF CRISPR-

Cas9 IN THE TREATMENT OF

CARDIOVASCULAR DISEASES

4.1 Off-Target Impacts

A significant concern in the clinical use of CRISPR-

Cas9 is off-target effects. The CRISPR-Cas9 system

may cleave DNA at locations other than the intended

target, leading to unintended genetic alterations.

These off-target events may have harmful

consequences, such as activation of oncogenes and

disruption of normal gene function. Studies have

shown that the frequency of off-target effects can be

relatively high (Shalem et al. 2015). Researchers have

created a number of tactics to deal with this problem,

one of which is creating high-fidelity Cas9 variations

like SpCas9-HF1. The purpose of these variations is

to lessen off-target activity. Another approach to

minimizing off-target effects is through the

optimization of sgRNA design. Studies have shown

that extending or truncating sgRNAs can enhance

genome editing fidelity. For instance, truncating

sgRNAs by 2-3 bp at the 5' end or putting two 5' end

guanine nucleotides (referred to as 5'-GGX20) can

decrease off-target effects while preserving on-target

efficiency. Lastly, off-target effects may also be

influenced by the way CRISPR-Cas9 components are

delivered. It has been demonstrated that lipid

nanoparticle (LNP) delivery and ribonucleoprotein

(RNP) electroporation produce fewer off-target

mutations and more on-target editing efficiency than

alternative techniques. In order to prevent prolonged

editor expression, which may result in off-target

consequences, these delivery approaches seek to

induce brief peak expression of CRISPR-Cas9

followed by rapid turnover.

4.2 Delivery Challenges

Another important drawback is the inability to

precisely transport CRISPR-Cas9 components to the

intended tissues in the cardiovascular system. Lipid

nanoparticles that carry mRNA expressing Cas9 and

gRNA are not very effective at delivering these

CRISPR-Cas9: A New Frontier in the Treatment and Research of Cardiovascular Diseases

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molecules, and they tend to build up in the liver and

spleen instead of targeting cardiac or muscle cells.

There are no specific markers for effective absorption

in cardiomyocytes. Although promising, AAV-based

methods for cardiac gene delivery are limited by pre-

existing immunity, immune responses, nonspecific

tissue transduction, high production costs, and limited

packaging capabilities. Dual AAV systems require

simultaneous infection of the same cell, which

reduces efficiency, and high doses raise safety

concerns.

4.3 Genome Stability and Immune

Responses

Unintentional genomic alterations brought on by

CRISPR-Cas9, like important deletions, intricate

rearrangements, and off-target effects, can be

harmful, particularly in cells that are undergoing

mitosis. Extensive DNA damage and loss of

heterozygosity can also have long-term

transcriptional effects that could activate

carcinogenic pathways (Bharucha et al. 2022).

Furthermore, a lot of people already have adaptive

immunity to S. aureus and S. pyogenes Cas9

orthologs. These immunological reactions raise the

possibility of immune-mediated adverse

consequences and reduce the effectiveness of gene

editing. Using immunoorthogonal Cas9 variations,

designing proteins with lower immunogenicity, and

using temporary immunosuppressive regimens are

some ways to deal with these problems (Bonowicz et

al. 2025). Furthermore, Cas9 can be temporarily

expressed by self-destruction or nonviral mRNA or

protein delivery, which can reduce the amount of time

needed for immune suppression. In summary, while

CRISPR-Cas9 technology holds great promise for

treating cardiovascular diseases, addressing delivery

challenges and ensuring genome stability and

immune compatibility are crucial steps towards its

clinical application. Ongoing research in these areas

is essential for CRISPR-Cas9 to reach its full

therapeutic potential.

5 FUTURE OUTLOOK AND

RESEARCH DIRECTIONS

5.1 Personalized Medicine

The combination of CRISPR-Cas9 and next-

generation sequencing holds great promise for

personalized medicine in the treatment of CVD. It is

possible to create curative treatments by precisely

altering pathogenic mutations in a patient's genome.

For instance, the paradigm of treatment for

hypertrophic cardiomyopathy might be completely

changed by fixing a single nucleotide mutation linked

to the condition. But there are issues with the healing

procedures that need to be resolved, such balancing

the error-prone NHEJ and HDR. In addition, issues

such as mosaicism, off-target effects, and ethical

concerns must be addressed before this approach can

be translated into clinical-scale treatments (Bharucha

et al. 2022).

5.2 Novel Delivery Systems

The widespread use of CRISPR-Cas9 in the treatment

of CVD depends on the creation of novel delivery

systems. Current research is focused on creating lipid

nanoparticles that target cardiovascular tissues, which

can enhance specificity and reduce off-target effects.

For example, the PuPGEA non-viral nanosystem has

demonstrated potential in delivering pCas9-Pcsk9

plasmids to hepatocytes, effectively knocking out the

Pcsk9 gene and reducing cholesterol levels. This

approach not only improves the efficiency of gene

delivery but also minimizes the risk of off-target

modifications and immune responses. To enhance

these delivery systems and guarantee their efficacy

and safety, more research is required. Using DNA

nanoclews, which are yarn-like DNA nanoparticles

produced by rolling circle amplification, is one

promising tactic. The Cas9 protein and single-guide

RNA (sgRNA) complexes can be encapsulated by

these nanoclews and delivered to human cell nuclei

while preserving cell viability. Another approach is

the development of cationic lipid-based delivery

systems, which have shown high transfection

efficiency in both vitro and vivo studies. These

systems can protect the CRISPR components from

degradation and facilitate their entry into cells,

thereby enhancing the overall efficacy of gene

editing.

In addition to these advancements, future research

should also focus on combining CRISPR-Cas9 with

other therapeutic modalities. For example,

integrating CRISPR technology with chimeric

antigen receptor (CAR)-T cell therapies could

enhance the efficacy of immunotherapy for CVD.

Moreover, the use of CRISPR-Cas9 for in vivo

editing of cardiovascular tissues could provide a

powerful tool for treating genetic heart diseases. In

conclusion, despite notable advancements in the

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development of CRISPR-Cas9 technology for the

treatment of CVD, ongoing research is crucial to

address the remaining challenges. By improving the

precision of CRISPR-Cas9 and developing more

efficient and targeted delivery systems, we can bring

new hope to patients with inherited cardiovascular

diseases, potentially leading to more effective and

personalized treatments. As technology advances, it

is essential to ensure that it is used in a way that

maximizes benefits and minimizes risks, both for

individuals and society.

6 CONCLUSION

CRISPR-Cas9 technology has made significant

progress in the treatment and research of

cardiovascular diseases. It has shown great potential

in correcting genetic mutations, regulating protein

expression, and targeting mitochondrial dysfunction

associated with CVD. In preclinical studies, it has

proven effective in treating various cardiovascular

diseases, such as familial hypercholesterolemia,

cardiomyopathy, and atherosclerosis. However,

challenges remain before CRISPR-Cas9 can be

widely implemented in clinical practice. Off-target

effects, delivery issues, genome stability concerns,

and immune responses are significant barriers.

Further research is essential to improve the precision

of CRISPR-Cas9 and develop more efficient and

targeted delivery systems. Overcoming these

obstacles will be crucial to ensuring both the safety

and effectiveness of CRISPR- Cas 9 based therapies.

In spite of these difficulties, the potential with

CRISPR-Cas9 to revolutionize cardiovascular

treatment is undeniable. With continued research and

development, it can bring new hope to patients with

inherited cardiovascular diseases, potentially leading

to more effective and personalized treatments. As the

technology develops, it is important to ensure that it

is used in a way that maximizes benefits and

minimizes risks, both for individuals and society.

REFERENCES

Amini, M., Zayeri, F., & Salehi, M. 2021. Trend analysis of

cardiovascular disease mortality, incidence, and

mortality-to-incidence ratio: results from global burden

of disease study 2017. BMC Public Health 21(1):401.

Bharucha, N., Arias, A., & Karakikes, I. 2022. The potential

of CRISPR-Cas9 prime editing for cardiovascular

disease research and therapy. Current Opinion in

Cardiology 37(5):413-418.

Bonowicz, K., Jerka, D., & Piekarska, K., et al. 2025.

CRISPR-Cas9 in Cardiovascular Medicine: Unlocking

New Potential for Treatment. Cells 14(2):131.

Cheng, K., Zhai, Q., & Song, J., et al. 2024. The Co-

pathogenic Target Gene CNTN1 Involved in Coronary

Artery Disease and Pulmonary Arterial Hypertension

Has Potential for Diagnosis of Coronary Artery

Disease. Anatolian Journal of Cardiology 28(8):381-

392.

Lee,Y.S., Choi, J.R., & Kim, J.B. 2024. Gene Therapy for

Cardiovascular Disease: Clinical Perspectives. Yonsei

Medical Journal 65(10):557-571.

Lloyd-Jones, D.M., Leip, E.P., & Larson, M.G., et al. 2006.

Prediction of lifetime risk for cardiovascular disease by

risk factor burden at 50 years of age. Circulation

113(6):791-798.

Morgan, M., Yellapu, V., & Short, D., et al. 2024. Trends

in In-Hospital Mortality in Patients Admitted With

Cardiovascular Diseases in the United States With

Demographics and Risk Factors of All Cardiovascular

In-Hospital Mortality: Analysis of the 2021 National

Inpatient Sample Database. Cureus Journal of Medical

Science 16(10):e70620.

Nammi, J.Y., Pasala, R., & Kotaru, S., et al. 2024.

Cardiovascular Disease Prevalence in Asians Versus

Americans: A Review of Genetics, Diet, and the Call

for Enhanced Prevention and Screening. Cureus Journal

of Medical Science 16(4):e58361.

Okobi, O.E., Nwogwugwu, E., Ihezie, C.O. 2024.

Cardiovascular Disease Patterns, Mortality, and

Hospitalization Trends in Adults Over 18: Insights

From the Behavioral Risk Factor Surveillance System

Database. Cureus Journal of Medical Science

16(8):e66604.

Shalem, O., Sanjana, N.E., Zhang, F. 2015. High-

throughput functional genomics using CRISPR-Cas9.

Nature Reviews Genetics (5):299-311.

Shojaei Baghini,S., Gardanova, Z.R., & Abadi, S.A.H., et

al. 2022. CRISPR/Cas9 application in cancer therapy: a

pioneering genome editing tool. Cellular & Molecular

Biology Letters 27(1):35.

Smolderen, K.G., Gillaspy, S., & Evers, A.W.M., et al.

2024. The Role of the Clinical Psychologist in the Care

of Adults With Cardiovascular Disease. Journal of the

American College of Cardiology Advances

3(4):100910.

Yang, L., Li, H., & Han, Y., et al. 2023. CRISPR/Cas9

Gene Editing System Can Alter Gene Expression and

Induce DNA Damage Accumulation. Genes 14(4):806.

CRISPR-Cas9: A New Frontier in the Treatment and Research of Cardiovascular Diseases

367