Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2023 Apr 26;13:6851. doi: 10.1038/s41598-023-33977-4

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

© The Author(s) 2023

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

PMC Copyright notice

Model depicting two distinct interpretations of nuclear LDs in liver diseases. Schematic representation of potential significance of LDs in the nucleus. Left model: in human hepatocytes under ER stress, secretion of VLDL can be suppressed, leading to accumulation of lipoprotein precursors in the ER lumen. These precursors then translocate into the lumen of type 1 NR (INM invagination), which results in increased amount of nLDs. The surface of nLDs can play a role in induction of PC synthesis to reduce ER stress in various liver diseases. Right model: alternatively, in hepatocytes of patients with low total and LDL cholesterol plasma levels, cholesterols will be sequestered in cellular membranes (e.g. in the NE), which may accelerate the formation type 2 NR (invagination of ONM and INM). cLDs may be initially packed in type 2 NR to be isolated from ER contact sites. This leads to decreased usage of lipids stored in cLDs for VLDL production in the ER. In these circumstances, cLDs in NR may negatively regulate the VLDL secretion machinery in hepatocytes. This machinery may be inhibited when patients’ liver show severe steatosis in which hepatocytes accumulate cholesterols as cholesterol esters in excessive cLDs instead of as free cholesterol in cellular membranes. cLDs in NR cytoplasmic lipid droplets in the nucleoplasmic reticulum, ER endoplasmic reticulum, INM inner nuclear membrane, LDL low-density lipoprotein, nLDs nucleoplasmic lipid droplets, NR nucleoplasmic reticulum, NE nuclear envelope, ONM outer nuclear membrane, PC phosphatydilcholine, VLDL very low-density lipoprotein.