Scope: Comprehensive review of ANGPTL3 inhibition as a therapeutic strategy to reduce triglyceride-rich lipoproteins and residual cardiovascular risk Therapeutic approaches discussed: Monoclonal antibodies (e.g., evinacumab) RNA-based therapies (ASOs and siRNA: vupanorsen, zodasiran, solbinsiran) Emerging gene-editing strategies (CRISPR/base editing) Key message: Targeting ANGPTL3 provides robust reductions in triglycerides, apoB-containing lipoproteins, and non-HDL cholesterol, independently of the LDL receptor Clinical relevance: Positions ANGPTL3 inhibition as a next-generation approach for managing mixed dyslipidemia and lipid-related residual risk beyond LDL-C Laura Schreier Natalia Nardelli European Atherosclerosis Society To view or add a comment, sign in Tipping the Scale in MASH: The TZD vs
It acts directly on the hypothalamus to stimulate the release of gonadotropin-releasing hormone (GnRH), which in turn triggers the pituitary gland to secrete LH and FSH
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GLP-1RA therapy was associated with reductions in total cholesterol, low-density lipoprotein cholesterol and triglyceride levels compared with placebo or other hypoglycaemic agents
