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Trends Cell Biol. 2014 Dec;24(12):743-50. doi: 10.1016/j.tcb.2014.06.006. Epub 2014 Jul 21.

Lysosome: regulator of lipid degradation pathways.

Author information

1
Dulbecco Telethon Institute, Via Pietro Castellino 111, 80131, Naples, Italy; Telethon Institute of Genetics and Medicine (TIGEM), Via Pietro Castellino 111, 80131, Naples, Italy; Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, TX, USA; Jan and Dan Duncan Neurological Research Institute, Texas Children's Hospital, Houston, TX, USA; Medical Genetics, Department of Translational and Medical Science, Federico II University, Via Pansini 5, 80131 Naples, Italy. Electronic address: Settembre@tigem.it.
2
Telethon Institute of Genetics and Medicine (TIGEM), Via Pietro Castellino 111, 80131, Naples, Italy; Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, TX, USA; Jan and Dan Duncan Neurological Research Institute, Texas Children's Hospital, Houston, TX, USA; Medical Genetics, Department of Translational and Medical Science, Federico II University, Via Pansini 5, 80131 Naples, Italy. Electronic address: Ballabio@tigem.it.

Abstract

Autophagy is a catabolic pathway that has a fundamental role in the adaptation to fasting and primarily relies on the activity of the endolysosomal system, to which the autophagosome targets substrates for degradation. Recent studies have revealed that the lysosomal-autophagic pathway plays an important part in the early steps of lipid degradation. In this review, we discuss the transcriptional mechanisms underlying co-regulation between lysosome, autophagy, and other steps of lipid catabolism, including the activity of nutrient-sensitive transcription factors (TFs) and of members of the nuclear receptor family. In addition, we discuss how the lysosome acts as a metabolic sensor and orchestrates the transcriptional response to fasting.

KEYWORDS:

Autophagy; FOXOs; TFEB; TP53; lipophagy; lysosome; mTORC1; nuclear receptors; transcription factors

PMID:
25061009
PMCID:
PMC4247383
DOI:
10.1016/j.tcb.2014.06.006
[Indexed for MEDLINE]
Free PMC Article

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