Autophagy in the endocrine glands

Abstract

Autophagy is an important cellular process involving the degradation of intracellular components. Its regulation is complex and while there are many methods available, there is currently no single effective way of detecting and monitoring autophagy. It has several cellular functions that are conserved throughout the body, as well as a variety of different physiological roles depending on the context of its occurrence in the body. Autophagy is also involved in the pathology of a wide range of diseases. Within the endocrine system, autophagy has both its traditional conserved functions and specific functions. In the endocrine glands, autophagy plays a critical role in controlling intracellular hormone levels. In peptide-secreting cells of glands such as the pituitary gland, crinophagy, a specific form of autophagy, targets the secretory granules to control the levels of stored hormone. In steroid-secreting cells of glands such as the testes and adrenal gland, autophagy targets the steroid-producing organelles. The dysregulation of autophagy in the endocrine glands leads to several different endocrine diseases such as diabetes and infertility. This review aims to clarify the known roles of autophagy in the physiology of the endocrine system, as well as in various endocrine diseases.

Overnutrition, mTOR signaling, and cardiovascular diseases

“…AMPK phosphorylation of Raptor causes Raptor's sequestration by 14-3-3 proteins, inactivating Raptor as a scaffolding molecule for mTORC1 and its downstream signaling pathways (43). There are several upstream kinases that can activate AMPK by phosphorylating a threonine residue on its catalytic ␣-subunit, such as liver kinase B1, calcium/calmodulin kinase, and TGF-␤-activated kinase-1 (63,84). Thus, by coupling AMPK activity with energy status, AMPK tightly regulates cellular function in various human physiological and pathological processes.…”

“…3). Indeed, increased levels of free fatty acids (FFAs) usually increase autophagic activity through inhibition of mTORC1, promoting activation of eukaryotic initiation factor 2 (eIF-2␣), and enhancing activation of PKC (84). However, dyslipidemia, a major characteristic of the CRS and diabetes, has been reported to impair the autophagic process.…”

Autophagy: A housekeeper in cardiorenal metabolic health and disease

“…Elongation of the autophagosome is mediated by two conjugated systems comprising Atg12–Atg5–Atg16 and LC3–phosphatidylethanolamine (PE). After formation of complete autophagic vesicles, the mature autophagosome becomes fused with a lysosome to create an autolysosome, where sequestered molecules and organelles are degraded [14,15]. Autophagosomes can directly fuse with lysosomes, or they can further receive inputs from the endocytic pathway and form hybrid organelles named amphisomes.…”

Autophagy in endocrine tumors

“…Since the involvement of autophagy in both physiological conditions and non-cancer pathologies of the ovaries and testes has been reported (Weckman et al 2014), and since autophagy appears to be important in non-endocrine ovarian cancer as well as in cancer of many other endocrine glands, it is likely that much remains to be discovered in this area.…”

“…Different types of autophagy, such as macroautophagy, microautophagy and chaperonemediated autophagy, have been described, each with different specific functions and slightly different mechanisms. All types of autophagy, however, share the end result of lysosome-mediated degradation of cytoplasmic components (Weckman et al 2014). The ubiquitous cellular process of autophagy has been explored in a wide array of different contexts, including both physiological and pathological conditions.…”