Submit a comment
Abstract
The liver plays a major role in regulating the metabolic fate of lipids and facilitates lipid secretion to peripheral organs in the form of VLDLs or lipid storage in lipid droplets (LDs). Hepatic regulation of excess lipids profoundly influences the development of atherosclerosis; thus, uncovering the regulatory mechanisms underlying lipid storage and secretion pathways may reveal additional therapeutic targets. In this issue of the JCI, Lu et al. identified a pathway involving SEC16B, showing that this protein functions as a lipid-responsive regulator and mediates VLDL secretion and LD formation to maintain lipid homeostasis. They also demonstrated that a reduction in SEC16B reduced serum lipid levels and atherosclerotic plaque area in Ldlr–/– mice. These results indicate that SEC16B connects VLDL and LD metabolism, positioning SEC16B as a potential therapeutic avenue for atherosclerosis.
Authors
Hossein Ardehali
Guidelines
The Editorial Board will only consider comments that are deemed relevant and of interest to readers. The Journal will not post data that have not been subjected to peer review; or a comment that is essentially a reiteration of another comment.
- Comments appear on the Journal’s website and are linked from the original article’s web page.
- Authors are notified by email if their comments are posted.
- The Journal reserves the right to edit comments for length and clarity.
- No appeals will be considered.
- Comments are not indexed in PubMed.
Specific requirements
- Maximum length, 400 words
- Entered as plain text or HTML
- Author’s name and email address, to be posted with the comment
- Declaration of all potential conflicts of interest (even if these are not ultimately posted); see the Journal’s conflict-of-interest policy
- Comments may not include figures
Copyright © 2026 American Society for Clinical Investigation
ISSN: 0021-9738 (print), 1558-8238 (online)