01
DOI: 10.1016/j.cmet.2024.07.014
02
Mitochondria, aptly nicknamed the cellular "powerhouses," are pivotal in energy metabolism, harnessing the tricarboxylic acid (TCA) cycle to unlock energy. Emerging research points to a calcium ion dependency within the TCA cycle's dehydrogenase enzymes, with the mitochondrial calcium uniporter (MCU) complex playing a key role by importing calcium ions into the mitochondrial matrix, thus amplifying the mitochondria's oxidative phosphorylation capabilities and energy yield. However, recent insights revealed that calcium fluctuations within the mitochondrial matrix mirror those of the cytoplasm, hinting at a potentially more substantial regulatory role for cytoplasmic calcium in oxidative phosphorylation. Despite this, the underlying mechanisms remain shrouded in mystery, and it is this enigma that the current study seeks to unravel. This investigation unveiled a novel regulatory mechanism in the context of MCU deficiency, where the cytoplasm's accumulated calcium ions steer hepatic lipid metabolism via the CAMKII-ATGL axis, leading to a reduction in hepatic lipid deposition. This discovery not only advanced our comprehension of the intricate interplay between calcium signaling and lipid homeostasis but also casted light on innovative avenues for exploring liver disease pathology. The findings are set to enrich the therapeutic landscape of liver-related disorders by shedding new light on the molecular underpinnings of conditions such as non-alcoholic fatty liver disease (NAFLD) and non-alcoholic steatohepatitis (NASH), potentially leading to the development of targeted.
DOI: https://doi.org/10.1016/j.cmet.2024.07.016
关注我们获取更多免疫学文献资讯
Editor & Reviewer: Congci Yu
