The diabetic population has a relatively high risk of developing hyperlipidemia, especially TRL dyslipidemia. Accumulating evidence points to the causal role of triglyceride lipoproteins and their cholesterol-enriched remnants in atherogenesis. The pathogenesis and mechanisms involve the ineffective TRL catabolism, the dysfunction of apolipoproteins, lipoprotein lipase (LPL) and its main regulators, such as the Apo CIII, Apo AV, and angiopoietin-like proteins in the partition of TRLs during the fast-fed cycle.
According to the pathophysiology and mechanisms of TRL metabolism, the therapeutic strategies might be different in terms of lipolysis, remodeling in the bloodstream, and clearance of remnant particles. Apo CIII and ANGPTL3 are now the main targets due to their roles in regulating LPL activity. However, previous triglyceride-lowering medications, including fibrates, nicotinic acid, and omega-3 PUFAs, had a broad range of effects but limited efficacy. It is urgent to screen new effective therapy for TRL lowering and gold standard method for measuring TRL remnants.
For this Research Topic, we welcome researchers to submit Original Research articles, Systematic Review as well as Review articles that will contribute to the field of TRL metabolism. We welcome basic and clinical studies focusing on the etiology, pathophysiology, measurements, and therapy of TRLs.
This Research Topic is interested in the following research fields, including but not limited to:
• Preclinical studies to explore the mechanisms of TRL dyslipidemia, including newly discovered role of apolipoproteins, dysfunction of LPL and its main regulators, such as the Apo CIII, Apo AV, and angiopoietin-like proteins
• New precise methods to measure the TRL remnants
• Mechanism study of the ultimate integration between the Apo CIII, Apo AV, and ANGPTL regulatory actions on LPL activity
• Role of LPLs in physiology and pathophysiology of the TRL dyslipidemia
• New therapeutic strategies to prevent, alleviate or reverse TRL dyslipidemia.
The diabetic population has a relatively high risk of developing hyperlipidemia, especially TRL dyslipidemia. Accumulating evidence points to the causal role of triglyceride lipoproteins and their cholesterol-enriched remnants in atherogenesis. The pathogenesis and mechanisms involve the ineffective TRL catabolism, the dysfunction of apolipoproteins, lipoprotein lipase (LPL) and its main regulators, such as the Apo CIII, Apo AV, and angiopoietin-like proteins in the partition of TRLs during the fast-fed cycle.
According to the pathophysiology and mechanisms of TRL metabolism, the therapeutic strategies might be different in terms of lipolysis, remodeling in the bloodstream, and clearance of remnant particles. Apo CIII and ANGPTL3 are now the main targets due to their roles in regulating LPL activity. However, previous triglyceride-lowering medications, including fibrates, nicotinic acid, and omega-3 PUFAs, had a broad range of effects but limited efficacy. It is urgent to screen new effective therapy for TRL lowering and gold standard method for measuring TRL remnants.
For this Research Topic, we welcome researchers to submit Original Research articles, Systematic Review as well as Review articles that will contribute to the field of TRL metabolism. We welcome basic and clinical studies focusing on the etiology, pathophysiology, measurements, and therapy of TRLs.
This Research Topic is interested in the following research fields, including but not limited to:
• Preclinical studies to explore the mechanisms of TRL dyslipidemia, including newly discovered role of apolipoproteins, dysfunction of LPL and its main regulators, such as the Apo CIII, Apo AV, and angiopoietin-like proteins
• New precise methods to measure the TRL remnants
• Mechanism study of the ultimate integration between the Apo CIII, Apo AV, and ANGPTL regulatory actions on LPL activity
• Role of LPLs in physiology and pathophysiology of the TRL dyslipidemia
• New therapeutic strategies to prevent, alleviate or reverse TRL dyslipidemia.
