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  • Advances in the Therapeutic Management of Hyperlipidaemia: Integrating Cholesterol Biology, Pharmacological Innovations, and Nanotechnology-Based Drug Delivery Systems

  • 1S. Y. M. Pharmacy, Department of Pharmaceutics, Konkan Gyanpeeth Rahul Dharkar College of Pharmacy and Research Institute, Karjat, Maharashtra, India. 
    2Assosiate Professor, Department of Pharmaceutics, Konkan Gyanpeeth Rahul Dharkar College of Pharmacy and Research Institute, Karjat, Maharashtra, India. 
    3Principal, Konkan Gyanpeeth Rahul Dharkar College of Pharmacy and Research Institute, Karjat, Maharashtra, India. 
    4Assistant Professor, Department of Pharmaceutics, Konkan Gyanpeeth Rahul Dharkar College of Pharmacy and Research Institute, Karjat, Maharashtra, India
     

Abstract

This comprehensive review elucidates the complex pathophysiological underpinnings and evolving therapeutic landscape of hyperlipidaemia, with a primary emphasis on the molecular biology of cholesterol metabolism and transport. It critically examines recent pharmacotherapeutic advances, including HMG-CoA reductase inhibitors and proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors, while also delineating the integration of nanotechnology-enabled drug delivery systems aimed at enhancing bioavailability and therapeutic efficacy. Furthermore, the article synthesizes contemporary clinical guidelines and explores the multifactorial influences of genetic predisposition, dietary intake, and dysregulated lipoprotein dynamics. Special attention is given to solubility enhancement strategies that address pharmacokinetic limitations of lipid-lowering agents, underscoring their relevance in optimizing clinical outcomes in hyperlipidaemic patients.

Keywords

Hyperlipidaemia, Cholesterol, Statins, PCSK9 inhibitors, Drug Delivery, Nanotechnology

Introduction

Introduction to Lipids

Cholesterol and triglycerides are the major plasma lipids present in the body which are essential for human health. Cholesterol is synthesized by the liver and is important component of the cell membranes serves as precursors to the bile acid and steroid hormones. Lipids are insoluble in water and they must be transported through blood in specialized complexes, called lipoproteins (Tabas 2002)

Cholesterol in Health and Disease

Cholesterol plays a vital role in maintaining cell membrane integrity, hormone production, and bile synthesis. However, its dysregulation is a key factor in the development of atherosclerosis, a leading cause of heart disease and stroke. (Tierona L.D. 2009)

Cholesterol Homeostasis

Cholesterol is obtained from dietary sources and synthesized endogenously. Its levels are tightly regulated through a balance of synthesis, uptake, efflux, and excretion. Lipoproteins such as LDL (low-density lipoprotein) and HDL (high-density lipoprotein) are crucial for its transport in the bloodstream.

  1. LDL: Often referred to as “bad cholesterol,” elevated LDL levels promote cholesterol deposition in arterial walls, forming plaques.
  2. HDL: Known as “good cholesterol,” HDL facilitates reverse cholesterol transport, removing cholesterol from tissues and plaques.

Atherosclerosis and Cholesterol

Atherosclerosis is a chronic inflammatory condition driven by cholesterol-laden macrophages (foam cells) in arterial walls. LDL oxidation and immune responses exacerbate plaque formation, eventually leading to vascular blockages or ruptures.

Cholesterol-Related Diseases

Beyond cardiovascular disease, dysregulated cholesterol contributes to conditions such as: Gallstones (due to cholesterol precipitation in bile), Neurodegenerativediseases (e.g., Alzheimer's, where cholesterol affects amyloid metabolism).

Therapeutic Interventions

Current therapies target cholesterol levels and inflammatory pathways, including:

  • Statins: Reduce cholesterol synthesis by inhibiting HMG-CoA reductase.
  • PCSK9 inhibitors: Enhance LDL receptor recycling, lowering LDL levels.
  • Lifestyle changes: Diet and exercise improve lipid profiles and overall cardiovascular health. (Tabas 2002)

Types of cholesterol:

1. Very low-density lipoprotein (VLDL): This cholesterol is composed of 50% to 65% glycerides and 20% to 30% cholesterol and is synthesized by the liver. It is responsible for transporting the triglycerides to adipose and muscular tissue.

2. Low density lipoprotein cholesterol: It is a cholesterol consists of a predominantly cholesterol inner core. It is obtained from the breakdown of the metabolites of VLDL. It is made up of 51% - 58% of cholesterol and 4% - 8% of triglycerides. The important function is to deliver the cholesterol from the liver cells.

3. High density lipoprotein (HDL): This type of cholesterol is a good cholesterol; it protects arterial disease from occurring as it takes away from the cells and back to liver. Once in the liver it is breakdown or excreted from the body in the form of waste. The HDL is the densest of lipoprotein. Other lipids that play a role in healthy arteries are chylomicrons and triglycerides. Hypelipidemia is a disease characterized by increased plasma lipids level may be due to genetic factors (primary) and secondary factors such as diabetes, hypothyroidism, and nephritic syndrome. The daily consumption of food provides required cholesterol and 20%-25% is synthesized by the liver. The remaining is synthesized by the intestine, adrenal glands, reproductive organs and other tissues. Elevated blood levels are harmful and lead to cardiovascular diseases. Particularly the low-density lipoproteins cholesterol (LDL), it deposited in the inner wall of large, medium sized arteries such as atherosclerotic plaque. This causes obstruction to the arteries, leads to the hypertension and reduction of oxygenated blood to which is reach to the heart and leads to increase the risk of coronary heart diseases, myocardium infarctions and cerebral arterials disease. The liver of an individual with average frame and weight synthesizes about 1000 mg of cholesterol daily. The total cholesterol content of the body is approximately 35 grams. It is transferred by the bile into the intestinal tract. About 50% of excreted cholesterol is reabsorbed by the digestive system and pumped back into circulation. This cholesterol recycling is continuous in nature. (Tierona L.D. 2009)

Fig. 1 Pictorial representation of cholesterol transport in the human body.

(A) Transport of dietary lipid in the form of TG, FFA, and cholesterol from the intestine to various organs, tissues, and cells. Dietary lipids or cholesterol are converted into chylomicrons with the help of bile acid. Chylomicrons shed TG & FFA, and the remaining chylomicron remnant containing cholesterol reaches the liver.

(B) Reverse cholesterol transport from organs, tissues, or cells and back to the liver. Reverse cholesterol transport is mediated by HDL to remove excess cholesterol from different organs/tissue, small “c” represents cholesterol

(C) Transport of TG, FFA, and cholesterol from the liver to other organs, tissues, and cells. The liver releases VLDLc consisting of different lipid components i.e., TG, FFA, and cholesterol. VLDLc shed TG & FFA forming IDLc and LDLc, cholesterol from LDLc is either used up by organs/tissue/cells or being taken up by the liver. (Mayengbam 2021)

Fig. 2 Major breakthroughs of cholesterol-related discoveries in chronological order. Landmark discoveries in cholesterol biology (Mayengbam 2021)

Fig. 3 Structure of cholesterol and its indispensable biological functions.

(A) Important biological functions of cholesterol. (B) Structure of cholesterol adopted from PubChem. Cholesterol is formed by 27 carbon atoms, 45 hydrogen atoms, and 1 hydroxyl group (C 27 H 46 O)

Causes of hyperlipidaemia:

Hyperlipidaemia is mainly due to genetic and environmental factors, including:

1) Presence of diseases such as diabetes, hypertension, hypertriglyceridemia, kidney and liver related diseases.

2) Family history to developing CHD or CVA early in their life (under 55 for brother and father and under 65 years of age for mother and sister).

3) Gender: Men have more risk to developing hyperlipidaemia compared to women.

4) Age: A person becomes older, so there may be chance for developing atherosclerosis.

5) Many foods like eggs, butter, liver, kidneys, and certain sea foods contain cholesterol, and other foods, like red meat, many cheeses, creamy cakes, ice cream, sausages and hot dogs have high contents of saturated fats and may affect to outcome of cholesterol blood concentration.

6) Sedentary lifestyle: It has been shown that non-vigorous physical activity leads to reduce LDL and elevate HDL blood levels. The bad habits such as smoking and over bodyweight are also responsible for hyperlipidaemia. (Tierona L.D. 2009)

7) Drugs: Thiazide Diuretics, Beta-Blockers, Glucocorticoids, Sex hormones, Retinoic Acid derivations, Antipsychotics, Antiretrovirals, Immunosuppressive agents. (Tierona L.D. 2009)

(Robert H Nelson a 2013)

Major risks of Hyperlipidaemias:

1. Atherosclerosis:

It is a disorder, occurs when the cholesterol, fat and calcium deposits in the arterial linings form multiple plaques. A plaque normally consists of three components Atheroma it is a fatty, soft, yellowish nodular mass deposit in the centre of a larger plaque that is consists of macrophages, which are the cells that play a role in immunity. A layer of cholesterol crystals. Calcified outer layer. Atherosclerosis leads to cardiovascular disease.

2. Coronary Artery Disease:

It is a condition which arteries are narrowing leads to less supply the blood to myocardium, and results in limiting blood flow and insufficient amounts of oxygen to meet the needs of the heart. The narrowing may progress to the extent that the heart muscle would sustain damage due to lack of blood supply.

3. Myocardial Infarction:

It is a condition, when blood and oxygen supplies are partially or completely blocked from flowing in one or more cardiac arteries, leads to damage or death of heart cells. The blockage is by formation of a clot in the artery. This condition is known as heart attack.

4. Angina Pectoris:

It is termed as angina; this condition is not a disease. This is characterized by chest pain, discomfort or a squeezing pressure. The pain may be felt in the shoulders, arms, neck and back. Angina is a condition occurs as a result of reduction or lack of blood supply to a part or the entire heart muscle and impairment of waste removal. Poor blood circulation is usually due to CHD when partial or complete obstruction of the coronary arteries is present. Angina attacks may be spasm of the arteries. Angina may be a symptom of coronary micro vascular disease (MVD), a condition that affects the heart’s smallest arteries.

4. Stroke (CVA):

This condition affects, when blood circulation of the brain is blocked. The blood supply which carries oxygen, glucose, and other nutrients is disrupted leads to brain cells die and become dysfunctional. Usually, the strokes occur due to blockage of artery by a blood clot that breaks loose in a small vessel within the brain. (Tierona L.D. 2009)

Treatment of Hyperlipidaemia:

Since lifestyle plays an important role in contributing to hyperlipidaemias, it more important to realize that TLC should be instituted and followed. The lowering of blood cholesterol level cannot be achieved alone, use of drugs becomes necessary.

  1. Lifestyle Modifications:

Adopting a whole-food, plant-based diet has been shown to be beneficial in preventing and treating hyperlipidaemia. A systematic review of 84 articles highlighted the effectiveness of such diets in improving cardiovascular risk factors, including lipid profiles. (Clebak and Dambro 2020)

  1. Pharmacological Treatments:
  1. Statins: These are the most commonly prescribed medications for lowering low-density lipoprotein cholesterol (LDL-C). They work by inhibiting HMG-CoA reductase, a key enzyme in cholesterol synthesis. Statins are recommended for adults aged 40-75 with at least one risk factor and a calculated 10-year cardiovascular disease risk of 10% or more. (Clebak and Dambro 2020)
  2. Ezetimibe: This medication reduces cholesterol absorption in the intestines and can be used alone or in combination with statins to achieve optimal lipid control.
  3. Bile Acid Sequestrants (BAS): These agents bind bile acids in the intestine, leading to increased cholesterol excretion. They are less frequently used due to gastrointestinal side effects.
  4. PCSK9 Inhibitors: These are monoclonal antibodies that enhance the liver's ability to remove LDL-C from the bloodstream. They are often used in patients who do not achieve lipid goals with statins alone. (Abbasi, Khan and Choudhry 2024)
  5. Bempedoic Acid: This is a newer agent that inhibits ATP citrate lyase, an enzyme involved in cholesterol synthesis, providing an alternative for patient’s intolerant to statins.
  6. Icosapent Ethyl: An omega-3 fatty acid derivative, it has been shown to reduce triglyceride levels and is associated with a reduction in major cardiovascular events. (Berberich and Hegele 2021)
  1. Statin are employed in the treatment of Hyperlipidaemia:

Statins, or HMG-CoA reductase inhibitors, are a cornerstone in managing hyperlipidaemia

A condition marked by elevated levels of lipids in the blood, notably low-density lipoprotein cholesterol (LDL-C). By inhibiting the enzyme HMG-CoA reductase, statins effectively reduce cholesterol synthesis in the liver, leading to decreased plasma LDL-C levels and a subsequent reduction in cardiovascular disease (CVD) risk.

Mechanism of Action of Statins:

Statins competitively inhibit HMG-CoA reductase, the enzyme responsible for converting HMG-CoA to mevalonate, a precursor in cholesterol biosynthesis. This inhibition lowers intracellular cholesterol levels, prompting an upregulation of LDL receptors on hepatocyte surfaces. The increased receptor expression enhances the clearance of circulating LDL-C, thereby reducing blood cholesterol levels.

Clinical Efficacy

The efficacy of statins in lowering LDL-C and reducing cardiovascular events is well-documented. A Cochrane review found that for every 1,000 individuals treated with a statin for five years, 18 would avoid major adverse cardiovascular events, including myocardial infarction, angina, or stroke. (Nelson 2013)

This benefit extends to both primary and secondary prevention of CVD.

Guideline Recommendations of authorities:

Clinical guidelines advocate for statin therapy in various populations:

  • Primary Prevention: The U.S. Preventive Services Task Force recommends statin use for adults aged 40 to 75 years with one or more CVD risk factors and a calculated 10-year CVD risk of 10% or greater.
  • Secondary Prevention: Individuals with established CVD benefit from statin therapy to prevent recurrent events. The 2018 American Heart Association/American College of Cardiology guidelines recommend high-intensity statin therapy for these patients. (Mangione, et al. 2022)

Safety and Adverse Effects of statins:

While generally well-tolerated, statins are associated with certain adverse effects:

  • Muscle-Related Symptoms: Myalgia and, less commonly, myopathy or rhabdomyolysis can occur. The incidence of statin-associated muscle symptoms (SAMS) varies, with severe muscle injury being rare.
  • Hepatotoxicity: Elevations in liver enzymes have been observed, though serious liver injury is uncommon. Routine monitoring of liver function tests is recommended during therapy.
  • New-Onset Diabetes: There is a modest increase in the risk of developing type 2 diabetes with statin use, particularly in individuals with predisposing risk factors. However, the cardiovascular benefits generally outweigh this risk. (Ward, Watts and Eckel 2019)

Comparative Efficacy of Different Statins

Various statins differ in their potency and lipid-modifying effects:

  • Atorvastatin and Rosuvastatin: These are considered high-potency statins, capable of achieving substantial reductions in LDL-C levels.
  • Simvastatin and Pravastatin: These have moderate potency and may be preferred in patients requiring less aggressive LDL-C lowering or those at increased risk for adverse effects. (Zhang, et al. 2020)

Special Populations of statins:

Chronic Kidney Disease (CKD): Statins are effective in reducing cardiovascular events in patients with CKD not requiring dialysis. However, their role in end-stage renal disease remains less clear.

Familial Hypercholesterolemia: Statins are a mainstay of treatment, though patients with homozygous familial hypercholesterolemia may require additional therapies to achieve target LDL-C levels. (Clebak and Dambro 2020)

Statins in Current Use:

Several statins are currently in clinical use, each varying in potency and pharmacokinetic properties:

  • Atorvastatin (Lipitor): Known for its high potency, atorvastatin can reduce LDL-C levels by more than 50% at high doses. (Nguyen 2024)
  • Rosuvastatin (Crestor): Another potent statin, rosuvastatin is effective in significantly lowering LDL-C and has a longer half-life, allowing for flexible dosing.
  • Simvastatin (Zocor): Effective in reducing LDL-C by up to 50% at moderate doses, simvastatin is often used when moderate cholesterol reduction is desired. The due to increased risk of myopathy the normal maintenance dose is 80 mg/day, usually during the first 20 month. The side effects include abdominal cramp, nausea, vomiting, diarrheas, flatulence, headache. Muscle weakness and myalgia was are rarely reported. The 20 mg/ day dosage is. usual initial dose for adult. A dose of 20 mg daily is initiated, this may be increased at intervals of not ? 4 weeks until a maximum dose of 80 mg is reached. (Nguyen 2024)
  • Pravastatin (Pravachol): Pravastatin has fewer drug interactions due to its minimal metabolism by the cytochrome P450 system, making it a safer option for patients on multiple medications.
  • Lovastatin (Mevacor): One of the earlier statins, lovastatin is effective in moderate LDL-C reduction but has a higher potential for drug interactions. The lovastatin occurs naturally and it is found in food such as oyster mushrooms, the FDA was approved the lovastatin first. After the oral administration presence of Food enhance the absorption rate. The side effects are abdominal pain, cramps, and dyspepsia, are usually. The dose of lovastatin different from one person to another person?s     and should determine the response of the patient and requirement of the patients. The normal maintenance dosage is 10 to 80 mg/ day given to the patients in a divided dose or single dosage. (Satish Ramkumar 2016)

New technologies/novel delivery systems for solubility enhancement

Enhancing the solubility of poorly water-soluble drugs is a significant challenge in pharmaceutical development. Recent advancements have introduced various technologies and delivery systems to address this issue.

  1. Nanotechnology-Based Approaches:

Nanotechnology has been pivotal in improving drug solubility and bioavailability. Nanoscale drug delivery systems (NDDSs) such as lipid-based carriers, polymer-based nanoparticles, nanoemulsions, nanogels, and inorganic carriers have demonstrated enhanced drug efficacy, targeted delivery, and reduced side effects. These systems are particularly beneficial for Biopharmaceutics Classification System (BCS) Class II and IV drugs, which suffer from low solubility and bioavailability. (Liu, et al. 2024)

  1. Solid Dispersion Techniques:

Solid dispersion involves dispersing poorly soluble drugs into a hydrophilic carrier matrix, enhancing dissolution rates and bioavailability. This method has been extensively studied and applied to improve the solubility of various drugs. (Shinkar, Patil and Saudagar 2017) Mesoporous Silica Carriers: Mesoporous silica has emerged as a promising carrier for amorphous solid dispersions (ASDs). Its nanosized capillaries and large surface area facilitate high drug loading and promote controlled release, thereby enhancing the solubility and stability of poorly soluble drugs. (Chaudhari and Gupte 2017)

  1. Self-Emulsifying Drug Delivery Systems (SEDDS):

SEDDS are isotropic mixtures of oils, surfactants, and solvents that spontaneously form emulsions upon contact with gastrointestinal fluids. They have shown significant potential in enhancing the solubility and oral bioavailability of hydrophobic drugs. (Hock, et al. 2021)

  1. Thiolated Polymers (Thiomer Technology):

Thiolated polymers, or thiomers, are a new generation of bio- and mucoadhesive polymers that form disulfide bonds with cysteine-rich subdomains of endogenous proteins. They have been utilized to improve drug solubility and mucoadhesion, leading to enhanced bioavailability. (Hock, et al. 2021) These innovative technologies offer promising solutions to the challenges posed by poorly soluble drugs, potentially leading to more effective and patient-friendly pharmaceutical formulations.

CONCLUSION
Hyperlipidemia remains a major modifiable risk factor for cardiovascular morbidity and mortality worldwide. An in-depth understanding of lipid and cholesterol metabolism has paved the way for significant advancements in therapeutic interventions. Traditional agents such as statins continue to be foundational, yet newer classes like PCSK9 inhibitors, ezetimibe, and bempedoic acid offer enhanced efficacy, particularly in high-risk and statin-intolerant populations. Moreover, emerging drug delivery technologies—especially nanotechnology-based systems—present promising avenues for improving solubility, bioavailability, and targeted delivery of lipid-lowering agents. Integration of lifestyle modifications, pharmacotherapy, and advanced formulation approaches represents a comprehensive strategy to optimize lipid control and mitigate cardiovascular risk. Continued research and innovation are essential to further refine these strategies and personalize treatment for diverse patient populations.

REFERENCES

  1. Abbasi, Seema, Adnan Khan, and Muhammad W. Choudhry. 2024. "New Insights into the Treatment of Hyperlipidemia: Pharmacological Updates and Emerging Treatments." Cureus (Springer Science and Business Media LLC). doi:10.7759/cureus.63078.
  2. Berberich, Amanda J., and Robert A. Hegele. 2021. "A Modern Approach to Dyslipidemia." Endocrine Reviews (The Endocrine Society) 43: 611–653. doi:10.1210/endrev/bnab037.
  3. Chaudhari, Smruti P., and Anshul Gupte. 2017. "Mesoporous Silica as a Carrier for Amorphous Solid Dispersion." (arXiv). doi:10.48550/ARXIV.1707.00036.
  4. Clebak, Karl T., and Anthony B. Dambro. 2020. "Hyperlipidemia: An Evidence-based Review of Current Guidelines." Cureus (Springer Science and Business Media LLC). doi:10.7759/cureus.7326.
  5. Giles, L. Amy. 2024. "Hyperlipidemia Prevention and Management Utilizing Lifestyle Changes." Journal of Midwifery & Women’s Health (Wiley) 69: 361–369. doi:10.1111/jmwh.13637.
  6. Hock, Nathalie, Giuseppe Francesco Racaniello, Sam Aspinall, Nunzio Denora, Vitaliy V. Khutoryanskiy, and Andreas Bernkop?Schnürch. 2021. "Thiolated Nanoparticles for Biomedical Applications: Mimicking the Workhorses of Our Body." Advanced Science (Wiley) 9. doi:10.1002/advs.202102451.
  7. Liu, Yifan, Yushan Liang, Jing Yuhong, Peng Xin, Jia Li Han, Yongle Du, Xinru Yu, et al. 2024. "Advances in Nanotechnology for Enhancing the Solubility and Bioavailability of Poorly Soluble Drugs." Drug Design, Development and Therapy (Informa UK Limited) Volume 18: 1469–1495. doi:10.2147/dddt. s447496.
  8. Mangione, Carol M., Michael J. Barry, Wanda K. Nicholson, Michael Cabana, David Chelmow, Tumaini Rucker Coker, Esa M. Davis, et al. 2022. "Statin Use for the Primary Prevention of Cardiovascular Disease in Adults: US Preventive Services Task Force Recommendation Statement." JAMA (American Medical Association (AMA)) 328: 746. doi:10.1001/jama.2022.13044.
  9. Mayengbam, Shyamananda Singh / Singh, Abhijeet / Pillai, Ajay D. / Bhat, Manoj Kumar. 2021. "Influence of cholesterol on cancer progression and therapy." Translational Oncology.
  10. Nelson, Robert H. 2013. "Hyperlipidemia as a Risk Factor for Cardiovascular Disease." Primary Care: Clinics in Office Practice (Elsevier BV) 40: 195–211. doi: 10.1016/j.pop.2012.11.003.
  11. Nguyen, Phuoc Anh (Anne). 2024. "Zocor (Simvastatin) vs. Lipitor (Atorvastatin): How Do They Compare?" verywell health.
  12. Robert H Nelson a, †. 2013. "Hyperlipidemia as a Risk Factor for Cardiovascular Disease." NIH Public Acces. doi: 10.1016/j.pop.2012.11.003.
  13. Satish Ramkumar, Ajay Raghunath and Sudhakshini Raghunath. 2016. "Statin Therapy: Review of Safety and Potential Side Effects." Acta Cardiol Sin.
  14. Shinkar, D. M., A. N. Patil, and R. B. Saudagar. 2017. "Review Article: Solubility Enhancement by Solid Dispersion." Asian Journal of Pharmacy and Technology (A and V Publications) 7: 72. doi:10.5958/2231-5713.2017.00011.3.
  15. Tabas, Ira. 2002. "Cholesterol in health and disease." Journal of Clinical Investigation (American Society for Clinical Investigation) 110: 583–590. doi:10.1172/jci0216381.
  16. Tierona L.D., and David Riley M.D. 2009. "Management of hyperlipidemia." Altern Ther Health Med. 9 (3): 28-41.
  17. Ward, Natalie C., Gerald F. Watts, and Robert H. Eckel. 2019. "Statin Toxicity: Mechanistic Insights and Clinical Implications." Circulation Research (Ovid Technologies (Wolters Kluwer Health)) 124: 328–350. doi:10.1161/circresaha.118.312782.
  18. Zhang, Xiaodan, Lu Xing, Xiaona Jia, Xiaocong Pang, Qian Xiang, Xia Zhao, Lingyue Ma, et al. 2020. "Comparative Lipid-Lowering/Increasing Efficacy of 7 Statins in Patients with Dyslipidemia, Cardiovascular Diseases, or Diabetes Mellitus: Systematic Review and Network Meta-Analyses of 50 Randomized Controlled Trials." Cardiovascular Therapeutics (Hindawi Limited) 2020: 1–21. doi:10.1155/2020/3987065.

Reference

  1. Abbasi, Seema, Adnan Khan, and Muhammad W. Choudhry. 2024. "New Insights into the Treatment of Hyperlipidemia: Pharmacological Updates and Emerging Treatments." Cureus (Springer Science and Business Media LLC). doi:10.7759/cureus.63078.
  2. Berberich, Amanda J., and Robert A. Hegele. 2021. "A Modern Approach to Dyslipidemia." Endocrine Reviews (The Endocrine Society) 43: 611–653. doi:10.1210/endrev/bnab037.
  3. Chaudhari, Smruti P., and Anshul Gupte. 2017. "Mesoporous Silica as a Carrier for Amorphous Solid Dispersion." (arXiv). doi:10.48550/ARXIV.1707.00036.
  4. Clebak, Karl T., and Anthony B. Dambro. 2020. "Hyperlipidemia: An Evidence-based Review of Current Guidelines." Cureus (Springer Science and Business Media LLC). doi:10.7759/cureus.7326.
  5. Giles, L. Amy. 2024. "Hyperlipidemia Prevention and Management Utilizing Lifestyle Changes." Journal of Midwifery & Women’s Health (Wiley) 69: 361–369. doi:10.1111/jmwh.13637.
  6. Hock, Nathalie, Giuseppe Francesco Racaniello, Sam Aspinall, Nunzio Denora, Vitaliy V. Khutoryanskiy, and Andreas Bernkop?Schnürch. 2021. "Thiolated Nanoparticles for Biomedical Applications: Mimicking the Workhorses of Our Body." Advanced Science (Wiley) 9. doi:10.1002/advs.202102451.
  7. Liu, Yifan, Yushan Liang, Jing Yuhong, Peng Xin, Jia Li Han, Yongle Du, Xinru Yu, et al. 2024. "Advances in Nanotechnology for Enhancing the Solubility and Bioavailability of Poorly Soluble Drugs." Drug Design, Development and Therapy (Informa UK Limited) Volume 18: 1469–1495. doi:10.2147/dddt. s447496.
  8. Mangione, Carol M., Michael J. Barry, Wanda K. Nicholson, Michael Cabana, David Chelmow, Tumaini Rucker Coker, Esa M. Davis, et al. 2022. "Statin Use for the Primary Prevention of Cardiovascular Disease in Adults: US Preventive Services Task Force Recommendation Statement." JAMA (American Medical Association (AMA)) 328: 746. doi:10.1001/jama.2022.13044.
  9. Mayengbam, Shyamananda Singh / Singh, Abhijeet / Pillai, Ajay D. / Bhat, Manoj Kumar. 2021. "Influence of cholesterol on cancer progression and therapy." Translational Oncology.
  10. Nelson, Robert H. 2013. "Hyperlipidemia as a Risk Factor for Cardiovascular Disease." Primary Care: Clinics in Office Practice (Elsevier BV) 40: 195–211. doi: 10.1016/j.pop.2012.11.003.
  11. Nguyen, Phuoc Anh (Anne). 2024. "Zocor (Simvastatin) vs. Lipitor (Atorvastatin): How Do They Compare?" verywell health.
  12. Robert H Nelson a, †. 2013. "Hyperlipidemia as a Risk Factor for Cardiovascular Disease." NIH Public Acces. doi: 10.1016/j.pop.2012.11.003.
  13. Satish Ramkumar, Ajay Raghunath and Sudhakshini Raghunath. 2016. "Statin Therapy: Review of Safety and Potential Side Effects." Acta Cardiol Sin.
  14. Shinkar, D. M., A. N. Patil, and R. B. Saudagar. 2017. "Review Article: Solubility Enhancement by Solid Dispersion." Asian Journal of Pharmacy and Technology (A and V Publications) 7: 72. doi:10.5958/2231-5713.2017.00011.3.
  15. Tabas, Ira. 2002. "Cholesterol in health and disease." Journal of Clinical Investigation (American Society for Clinical Investigation) 110: 583–590. doi:10.1172/jci0216381.
  16. Tierona L.D., and David Riley M.D. 2009. "Management of hyperlipidemia." Altern Ther Health Med. 9 (3): 28-41.
  17. Ward, Natalie C., Gerald F. Watts, and Robert H. Eckel. 2019. "Statin Toxicity: Mechanistic Insights and Clinical Implications." Circulation Research (Ovid Technologies (Wolters Kluwer Health)) 124: 328–350. doi:10.1161/circresaha.118.312782.
  18. Zhang, Xiaodan, Lu Xing, Xiaona Jia, Xiaocong Pang, Qian Xiang, Xia Zhao, Lingyue Ma, et al. 2020. "Comparative Lipid-Lowering/Increasing Efficacy of 7 Statins in Patients with Dyslipidemia, Cardiovascular Diseases, or Diabetes Mellitus: Systematic Review and Network Meta-Analyses of 50 Randomized Controlled Trials." Cardiovascular Therapeutics (Hindawi Limited) 2020: 1–21. doi:10.1155/2020/3987065.

Photo
Chitrang Patil
Corresponding author

S. Y. M. Pharmacy, Department of Pharmaceutics, Konkan Gyanpeeth Rahul Dharkar College of Pharmacy and Research Institute, Karjat, Maharashtra, India.

Photo
Dr. Nilesh Gorde
Co-author

Assosiate Professor, Department of Pharmaceutics, Konkan Gyanpeeth Rahul Dharkar College of Pharmacy and Research Institute, Karjat, Maharashtra, India.

Photo
Dr. Mohan Kale
Co-author

Principal, Konkan Gyanpeeth Rahul Dharkar College of Pharmacy and Research Institute, Karjat, Maharashtra, India.

Photo
Swapnil Phalak
Co-author

Assistant Professor, Department of Pharmaceutics, Konkan Gyanpeeth Rahul Dharkar College of Pharmacy and Research Institute, Karjat, Maharashtra, India

Chitrang Patil*, Dr. Nilesh Gorde, Dr. Mohan Kale, Swapnil Phalak, Advances in the Therapeutic Management of Hyperlipidaemia: Integrating Cholesterol Biology, Pharmacological Innovations, and Nanotechnology-Based Drug Delivery Systems, Int. J. of Pharm. Sci., 2025, Vol 3, Issue 5, 1200-1209. https://doi.org/10.5281/zenodo.15363257

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