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REFLECTIONS
Dyslipidaemia
Dyslipidaemia Global Newsletter #10 2025
support tools, patient education, and incentives for large-scale
production, along with a “rebranding” effort to build public and Dyslipidaemia
institutional trust, similar to how fixed-dose combinations were
successfully adopted in HIV/AIDS programs.
CLICK HERE
LISTEN TO JACC’S EDITOR-IN-CHIEF
CLICK HERE DR. HARLAN KRUMHOLZ SUMMARISE
FOR THE LINK TO FULL ARTICLE THIS STUDY (1:12-2:33).
The evolving landscape of targets for lipid lowering: From molecular mechanisms
to translational implications.
Ballantyne CM, et al. Eur Heart J. 2025 Sep 5;ehaf606. doi: https://doi.org/10.1093/eurheartj/ehaf606. Online ahead of print.
Dyslipidaemia remains a major contributor to CVD, and while lowering LDL-C is the primary target for prevention, significant residual
risk persists. This risk is driven by other factors, including TGs, apoB, and Lp(a). Furthermore, apoB, which reflects the number of
atherogenic particles, is considered a superior predictor of CVD risk compared to LDL-C or TG levels alone. This review looks to
discuss current and novel LLTs from a pharmacological and clinical perspective, focusing on the mechanism of action and expected
benefits in patients with CVD.
Graphical abstract
ACLY, ATP citrate lyase; ASGPR, asialoglycoprotein receptor; ATP, adenosine triphosphate; CETP, cholesteryl ester transfer protein; HMG-CoAR, 3-hydroxy-3-
methylglutaryl coenzyme A reductase; NPC1L1, Niemann-Pick C1-like 1; RISC, RNA-induced silencing complex; VLDL, very-low-density lipoprotein; acetyl-CoA,
acetyl coenzyme A.
TABLE OF CONTENTS
