Pharmacological agents:

• Statins

• Bempedoic acid

• PCSK9 inhibitors

• Inclisiran

• Niacin

• Fibrates

• Bile acid sequestrants

• ANGPTL3 inhibitors

Detailed Illustration of the lipoprotein metabolism in the human body. Chol: Cholesterol, CM: Chylomicrons, CMR: Chylomicrone Remnants, TAG: Triacylglycerol, FFA: Free Fatty Acids, HDL: High Density lipoprotein, LDL: Low Density Lipoprotein, VLDL: Very Low Density Lipoprotein, LPL: Lipoprotein Lipase, HL: Hepatic Lipase, LCAT: Lecithin cholesterol acyltransferase, CETP: Cholesteryl ester transfer protein, LDLR: LDL-Receptor

Detailed Illustration of intracellular Lipid Metabolism. HMG-CoA-R: HMG-CoA-Reductase, ATGL: Adipose Triglyceride Lipase, HSL: Hormone Sensitive Lipase, MGL: Monoglyceride Lipase, FA: Fatty Acids, ACL: ATP-Citrate-Lyase

The solution will be provided at the end of the clinical pearl. First, we are going to highlight each treatment options including their clinical implications in detail.

Management of dyslipidemia relies on a combination of lifestyle interventions and pharmacological therapies. The decision to initiate drug treatment, as well as the choice and intensity of therapy, is guided by the individual patient’s risk for lipid-related complications, including atherosclerotic cardiovascular disease and pancreatitis. In patients at elevated risk, pharmacological therapy is often introduced concurrently with lifestyle modification rather than sequentially.

Because lipid-lowering agents differ substantially in their mechanisms of action, selection of a specific therapy should be tailored to the underlying lipid abnormality and informed by practical considerations such as patient preferences, drug availability, regulatory approval, and reimbursement constraints. In the following sections, the mechanisms of action of the major therapeutic classes used in dyslipidemia will be reviewed and contextualized to illustrate how physiological targeting translates into clinical lipid profile improvement.

Lifestyle Modification

Lifestyle modification, particularly structured exercise and targeted dietary changes, forms the cornerstone of dyslipidemia management and is endorsed as first-line therapy by major professional societies, including the Endocrine Society and the American Association of Clinical Endocrinology.

Regular physical activity, encompassing both aerobic exercise and resistance training, produces modest yet clinically meaningful improvements in circulating lipids. Aerobic or combined exercise programs typically reduce LDL-C, total cholesterol, and triglycerides by roughly 3–12%, while increasing HDL-C by approximately 2–3 mg/dL. These effects scale with training intensity, session duration, and long-term adherence.

Dietary modification also affects lipid parameters. According to the American College of Cardiology, replacing saturated with unsaturated fats and limiting dietary cholesterol can lower LDL-C concentrations by about 10–15%. Interventions targeting triglyceride levels, such as carbohydrate restriction, weight reduction, and limiting added sugars and alcohol, can yield triglyceride reductions in the range of 16–42%, with the largest improvements observed in individuals achieving substantial weight loss or adhering to very-low-carbohydrate diets.

Pharmacological Agents Primarily Targeting Cholesterol Reduction

Inhibition of Hepatic Cholesterol Synthesis

Statins

Statins reduce circulating cholesterol concentrations by competitively inhibiting 3-hydroxy-3-methylglutaryl–coenzyme A (HMG-CoA) reductase, the rate-limiting enzyme in hepatic cholesterol synthesis. Suppression of endogenous cholesterol production lowers intracellular cholesterol content within hepatocytes, which in turn activates sterol regulatory element–binding protein 2 (SREBP-2). This transcriptional response leads to increased expression of LDL receptor genes and a higher density of LDL receptors on the hepatocyte surface. Enhanced receptor-mediated uptake of LDL particles from the circulation results in a pronounced reduction in plasma LDL cholesterol levels.

Illustration: How Statins influence intracellular Lipid Metabolism. HMG-CoA-R: HMG-CoA-Reductase, ATGL: Adipose Triglyceride Lipase, HSL: Hormone Sensitive Lipase, MGL: Monoglyceride Lipase, FA: Fatty Acids, ACL: ATP-Citrate-Lyase

Illustration: How Statins influence the lipoprotein metabolism in the human body. Chol: Cholesterol, CM: Chylomicrons, CMR: Chylomicrone Remnants, TAG: Triacylglycerol, FFA: Free Fatty Acids, HDL: High Density lipoprotein, LDL: Low Density Lipoprotein, VLDL: Very Low Density Lipoprotein, LPL: Lipoprotein Lipase, HL: Hepatic Lipase, LCAT: Lecithin cholesterol acyltransferase, CETP: Cholesteryl ester transfer protein, LDLR: LDL-Receptor

Bempedoic Acid

Bempedoic acid is an orally administered, once-daily prodrug that is selectively activated in hepatocytes. Its active metabolite inhibits ATP-citrate lyase, an enzyme positioned upstream of HMG-CoA reductase in the hepatic cholesterol biosynthetic pathway. By reducing intracellular cholesterol availability in the liver, bempedoic acid induces upregulation of LDL receptor expression, thereby enhancing receptor-mediated clearance of LDL particles from the circulation and lowering plasma LDL cholesterol concentrations.

Illustration: How Bempedoic Acid influences intracellular Lipid Metabolism. HMG-CoA-R: HMG-CoA-Reductase, ATGL: Adipose Triglyceride Lipase, HSL: Hormone Sensitive Lipase, MGL: Monoglyceride Lipase, FA: Fatty Acids, ACL: ATP-Citrate-Lyase

Modulation of the PCSK9–LDL Receptor Axis

Proprotein convertase subtilisin/kexin type 9 (PCSK9) is predominantly synthesized in the liver and plays a central role in regulating LDL receptor (LDLR) turnover. By binding to LDLRs on the hepatocyte surface, PCSK9 directs the receptor–ligand complex toward lysosomal degradation, thereby reducing the number of LDLRs available for clearance of circulating LDL cholesterol.

PCSK9 monoclonal antibodies
PCSK9 inhibitors, including alirocumab and evolocumab, are monoclonal antibodies administered subcutaneously that bind circulating PCSK9 and prevent its interaction with LDLRs. By blocking PCSK9-mediated receptor degradation, these agents preserve LDLR expression on the hepatocyte surface, leading to enhanced receptor-mediated uptake of LDL particles from plasma and marked reductions in LDL-C levels. In addition to LDL-C lowering, PCSK9 monoclonal antibodies reduce apolipoprotein B and lipoprotein(a) concentrations. While pleiotropic anti-inflammatory or anti-atherosclerotic effects have been proposed, their primary therapeutic action remains augmentation of LDLR availability and LDL-C clearance.

Inclisiran
Inclisiran lowers LDL cholesterol by suppressing hepatic PCSK9 production through RNA interference. It consists of a synthetic small interfering RNA (siRNA) conjugated to N-acetylgalactosamine, enabling selective uptake by hepatocytes via asialoglycoprotein receptors. Following cellular entry, the guide strand of inclisiran is incorporated into the RNA-induced silencing complex, which binds PCSK9 mRNA and promotes its degradation. This post-transcriptional silencing prevents PCSK9 protein synthesis, resulting in sustained reductions in circulating PCSK9 levels, preservation of LDL receptors, and enhanced clearance of LDL cholesterol.

Illustration: How PCSK9 Modulators influence the lipoprotein metabolism in the human body. Chol: Cholesterol, CM: Chylomicrons, CMR: Chylomicrone Remnants, TAG: Triacylglycerol, FFA: Free Fatty Acids, HDL: High Density lipoprotein, LDL: Low Density Lipoprotein, VLDL: Very Low Density Lipoprotein, LPL: Lipoprotein Lipase, HL: Hepatic Lipase, LCAT: Lecithin cholesterol acyltransferase, CETP: Cholesteryl ester transfer protein, LDLR: LDL-Receptor. Note: PCSK9-inhibiting antibodies bind on the LDL-R on the cell surface. Due to illusrative reasons, the mechanism of action is illustrated within the liver.

Intestinal Cholesterol-Uptake Inhibitors

Ezetimibe
Ezetimibe reduces cholesterol absorption at the level of the intestinal brush border by targeting the Niemann-Pick C1-like 1 (NPC1L1) transporter. NPC1L1 is a multipass transmembrane protein on the apical surface of enterocytes that mediates the uptake of both dietary and biliary cholesterol. By binding to NPC1L1 and preventing the conformational changes required for its endocytosis, ezetimibe effectively blocks cholesterol entry into the enterocyte. As a result, less cholesterol is delivered to the liver, leading to a compensatory decline in hepatic cholesterol stores. This reduction triggers upregulation of LDL receptor expression, thereby enhancing the clearance of LDL particles from the circulation.

Bile acid sequestrants
Bile acid sequestrants (e.g., cholestyramine, colesevelam) exert their effect by binding bile acids within the intestinal lumen, thereby preventing their reabsorption in the distal ileum and disrupting the enterohepatic circulation. Loss of bile acids prompts the liver to increase bile acid synthesis, primarily through upregulation of cholesterol 7α-hydroxylase, the rate-limiting enzyme in this pathway. The heightened demand for cholesterol drives increased hepatic LDL receptor expression, resulting in greater removal of LDL cholesterol from plasma. These agents act locally in the gut and are not systemically absorbed.

Illustration: How gastrointestinal cholesterol uptake inhibitors influence the lipoprotein metabolism in the human body. Chol: Cholesterol, CM: Chylomicrons, CMR: Chylomicrone Remnants, TAG: Triacylglycerol, FFA: Free Fatty Acids, HDL: High Density lipoprotein, LDL: Low Density Lipoprotein, VLDL: Very Low Density Lipoprotein, LPL: Lipoprotein Lipase, HL: Hepatic Lipase, LCAT: Lecithin cholesterol acyltransferase, CETP: Cholesteryl ester transfer protein, LDLR: LDL-Receptor.

Pharmacological Agents Primarily Targeting Triglyceride Reduction

Modulator of Lipoprotein Lipase Activity

Fibrates
Fibrates exert their lipid-modifying effects primarily through activation of peroxisome proliferator–activated receptor alpha (PPARα), a nuclear receptor that regulates the transcription of genes central to lipid and lipoprotein metabolism. PPARα activation increases expression of lipoprotein lipase (LPL), thereby enhancing the intravascular hydrolysis of triglyceride-rich lipoproteins, including very-low-density lipoproteins (VLDL) and chylomicrons. This mechanism results in a marked reduction in plasma triglyceride concentration. In parallel, fibrates reduce hepatic production of apolipoprotein C-III, an endogenous inhibitor of LPL, further facilitating triglyceride clearance. Additional effects include decreased hepatic VLDL secretion, mediated by increased fatty acid β-oxidation and reduced de novo lipogenesis. Collectively, these actions lower circulating triglycerides and remnant lipoproteins.

Illustration: How Fibrates influence the lipoprotein metabolism in the human body. Chol: Cholesterol, CM: Chylomicrons, CMR: Chylomicrone Remnants, TAG: Triacylglycerol, FFA: Free Fatty Acids, HDL: High Density lipoprotein, LDL: Low Density Lipoprotein, VLDL: Very Low Density Lipoprotein, LPL: Lipoprotein Lipase, HL: Hepatic Lipase, LCAT: Lecithin cholesterol acyltransferase, CETP: Cholesteryl ester transfer protein, LDLR: LDL-Receptor.

Illustration: How Fibrates influence intracellular Lipid Metabolism. HMG-CoA-R: HMG-CoA-Reductase, ATGL: Adipose Triglyceride Lipase, HSL: Hormone Sensitive Lipase, MGL: Monoglyceride Lipase, FA: Fatty Acids, ACL: ATP-Citrate-Lyase

Inhibitors of Hepatic VLDL Production

Omega-3 fatty acids
Omega-3 polyunsaturated fatty acids, particularly eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), lower plasma triglyceride concentrations predominantly by attenuating hepatic VLDL-triglyceride synthesis. This reduction is achieved through decreased availability of triglyceride substrates and downregulation of genes involved in lipogenesis. In addition, omega-3 fatty acids may modestly enhance the clearance of triglyceride-rich lipoproteins, potentially through increased lipoprotein lipase–mediated hydrolysis. Collectively, these effects result in a clinically meaningful reduction in circulating triglyceride levels.

Niacin (nicotinic acid)
Niacin primarily modulates lipid metabolism by suppressing hepatic triglyceride synthesis and subsequent very-low-density lipoprotein (VLDL) secretion. This effect is mediated in part through inhibition of diacylglycerol acyltransferase-2, a key enzyme involved in triglyceride assembly within hepatocytes. Reduced VLDL output leads to downstream decreases in circulating VLDL and LDL cholesterol concentrations. In addition, niacin favorably influences high-density lipoprotein metabolism by diminishing hepatic clearance of apolipoprotein A-I, thereby extending HDL particle residence time and increasing HDL-C levels. This mechanism supports enhanced reverse cholesterol transport.

Illustration: How VLDL-Inhibitors influence the lipoprotein metabolism in the human body. Chol: Cholesterol, CM: Chylomicrons, CMR: Chylomicrone Remnants, TAG: Triacylglycerol, FFA: Free Fatty Acids, HDL: High Density lipoprotein, LDL: Low Density Lipoprotein, VLDL: Very Low Density Lipoprotein, LPL: Lipoprotein Lipase, HL: Hepatic Lipase, LCAT: Lecithin cholesterol acyltransferase, CETP: Cholesteryl ester transfer protein, LDLR: LDL-Receptor.

Pharmacological Agents Targeting Triglyceride and Cholesterol Reduction

Modulator of Lipoprotein Lipase Activity

ANGPTL3 inhibitors
Angiopoietin-like protein 3 (ANGPTL3) is a hepatically derived regulator of lipid metabolism that suppresses the activity of both lipoprotein lipase and endothelial lipase, often in coordination with ANGPTL8. This inhibition promotes accumulation of triglyceride-rich lipoproteins and contributes to elevations in plasma triglycerides and LDL cholesterol. Pharmacological inhibition of ANGPTL3, achieved through monoclonal antibodies, antisense oligonucleotides, or small interfering RNA, releases this brake on lipase activity. The resulting increase in LPL function accelerates the clearance of VLDL, chylomicrons, and their remnants, leading to substantial reductions in plasma triglycerides, remnant cholesterol, and decreases in LDL-C. Importantly, LDL-C lowering via ANGPTL3 inhibition occurs independently of the LDL receptor pathway, rendering this approach particularly relevant for patients with homozygous familial hypercholesterolemia.

Illustration: How ANGPTL3-Inhibitors influence the lipoprotein metabolism in the human body. Chol: Cholesterol, CM: Chylomicrons, CMR: Chylomicrone Remnants, TAG: Triacylglycerol, FFA: Free Fatty Acids, HDL: High Density lipoprotein, LDL: Low Density Lipoprotein, VLDL: Very Low Density Lipoprotein, LPL: Lipoprotein Lipase, HL: Hepatic Lipase, LCAT: Lecithin cholesterol acyltransferase, CETP: Cholesteryl ester transfer protein, LDLR: LDL-Receptor.

Concluding Remarks: Translating Lipid Pathophysiology into Clinical Practice and Solution to the Exercise at the beginning of the Clinical Pearl

Understanding the physiology and pathophysiology of lipid metabolism is essential for selecting the most appropriate treatment strategy for dyslipidemia. Lipid abnormalities arise from distinct disturbances in cholesterol synthesis, intestinal absorption, lipoprotein production, clearance, and intravascular remodeling, and each therapeutic class targets a specific component of these pathways. Knowledge of where a dysregulation occurs allows clinicians to align lifestyle interventions and pharmacological therapies with the dominant lipid abnormality, such as elevated LDL cholesterol, hypertriglyceridemia, or mixed dyslipidemia, thereby maximizing efficacy while minimizing unnecessary exposure to ineffective treatments. Moreover, mechanistic insight helps anticipate treatment limitations, adverse effects, and drug interactions, and supports rational combination therapy in high-risk patients. Ultimately, a physiology-based approach enables individualized, evidence-informed management of dyslipidemia and optimizes cardiovascular risk reduction.

Detailed Illustration of the lipoprotein metabolism with mechanism of action of the most important pharmacological agents to treat dyslipidemia. Chol: Cholesterol, CM: Chylomicrons, CMR: Chylomicrone Remnants, TAG: Triacylglycerol, FFA: Free Fatty Acids, HDL: High Density lipoprotein, LDL: Low Density Lipoprotein, VLDL: Very Low Density Lipoprotein, LPL: Lipoprotein Lipase, HL: Hepatic Lipase, LCAT: Lecithin cholesterol acyltransferase, CETP: Cholesteryl ester transfer protein, LDLR: LDL-Receptor. Note: PCSK9-inhibiting antibodies bind on the LDL-R on the cell surface. Due to illusrative reasons, the mechanism of action is illustrated within the liver.

Detailed Illustration of intracellular Lipid Metabolism with mechanism of action of the most important pharmacological agents to treat dyslipidemia. HMG-CoA-R: HMG-CoA-Reductase, ATGL: Adipose Triglyceride Lipase, HSL: Hormone Sensitive Lipase, MGL: Monoglyceride Lipase, FA: Fatty Acids, ACL: ATP-Citrate-Lyase

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All Illustrations were created in https://BioRender.com

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