Key result
Liver-derived apolipoprotein B containing lipoproteins elicit atherosclerotic inflammatory sequelae comparable to LDL, serving as potential therapeutic targets for CVD prevention in NAFLD.
Why the study?
Understanding mechanisms linking liver-derived ApoB lipoproteins with inflammation is needed because current therapies lowering these lipoproteins have not achieved robust CVD risk reduction.
Liver-derived lipoproteins and their remnants play a key role in atherosclerotic inflammation, representing important therapeutic targets for CVD prevention in patients with metabolic liver diseases like NAFLD.
May identify remnant lipoproteins as CVD targets in NAFLD; hypothesis-generating and requires prospective validation.
Low density lipoproteins (LDL) reduction remains the key goal for reducing the risk of atherosclerotic cardiovascular diseases (CVD) in people with high residual risk and metabolic complications including liver disease. Notwithstanding, epidemiological projections support a key role of liver-derived apolipoprotein B (ApoB) containing lipoproteins, namely very low density lipoproteins (VLDL) and their “remnants” (TG), undergoing the activity of lipases, in eliciting atherosclerotic inflammatory sequelae of a comparable order of magnitude to that of LDL. Disparate experimental evidence supports that triglycerides (TG), residual cholesterol content, or the large apolipoprotein set on the surface of these lipoproteins can elicit a number of plausible immune-inflammatory mechanisms that foster the vascular atherosclerotic process. Therapeutic options that convincingly lowered the plasma levels of liver-derived ApoB containing lipoproteins, either by reducing the hepatic synthesis or by improving the peripheral lipolysis of the lipid content, did not exert robust CVD risk reduction, and the effect on inflammation was questionable. Understanding the mechanisms linking liver-derived lipoproteins with chronic inflammation will provide pathophysiological insights for the identification of new therapeutic targets for people at high CVD risk and with metabolic complications. In this perspective, this topic is of immediate interest for the prevention of CVD in patients affected by non-alcoholic fatty liver disease (NAFLD) and, even more, for NAFLD patients with diabetes, insulin resistance, or other comorbidities (metabolic-associated fatty liver disease). This review resumes the principal physio-pathological insights regarding the metabolism of liver-derived lipoproteins and provides an update on the current pharmacological options that can be considered for improving CVD prevention in metabolic liver diseases.
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Andrea Baragetti (2022) conducted a review in Metabolic liver disease and atherosclerotic cardiovascular disease. Pharmacological options targeting liver-derived lipoproteins was evaluated. Liver-derived apolipoprotein B containing lipoproteins elicit atherosclerotic inflammatory sequelae comparable to LDL, serving as potential therapeutic targets for CVD prevention in NAFLD.
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