Table 1.
Autophagy modulation of selected neuropeptides.
| Compound | Role on autophagy | Targets (cell/tissue) | Effects of neuropeptides∗ | Potential therapeutic applications |
|---|---|---|---|---|
| PACAP | Inhibition | Human SH-SY5Y cells; mouse brain | Decreasing apoptosis; preservation of mitochondrial activity; neuroprotection | Parkinson disease |
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| SP | Activation(?) | Mouse skin; Wistar rat bladder | Hair cycle alteration; apoptosis | Psychological stress conditions; bladder disorders |
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| NPY | Activation | Rat/mouse cortical/hypothalamic neurons; mouse hypothalamus | Neuroprotection | Control of feeding; metabolic syndrome; aging; neurodegenerative diseases |
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| Ghrelin | Activation | Mouse skeletal muscle; rat cortical neurons | Restoring insulin signalling; neuroprotection | Diabetes; aging |
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| Ghrelin | Inhibition | Rat H9c2 cells; human HO-8910 cells; mouse liver | Cell survival and size maintenance; reducing cell proliferation; apoptosis; decreasing expression of pathological markers | Heart failure; ovarian cancer; liver fibrosis |
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| Leptin | Activation | Human HepG2 cells; human MCF-7 cells; HepG2 tumour xenografts | Tumour growth; tumour invasion; decreasing apoptosis | Obesity-associated breast and hepatic cancers |
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| SRIF | Activation | Human GH-secreting adenomas | Decreasing cell proliferation | Acromegaly |
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| Orexin A | Activation | Human HCT-116 cells | Decreasing cell viability | Colon cancer |
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| Ang-II | Activation | Human HUVEC cells; rat vascular smooth cells; mouse podocytes; rat cardiomyocytes | Cell senescence; apoptosis; production of reactive oxygen species§; cardiomyocyte hypertrophy | Cardiovascular diseases; heart failure; proteinuria |
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| Intermedin | Activation(?) | Rat H9c2 cells; mouse hearts | Attenuation of myocardial infarction; cardiomyocyte survival; improvement of cardiac performance | Heart failure; cardiac hypertrophic diseases |
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| Urocortin 1 | Inhibition | Rat cardiomyocytes | Decreasing apoptosis | Heart failure |
∗In some cases these effects have been clearly demonstrated to be dependent on neuropeptide-induced modulation of autophagy. §It has been hypothesised that autophagy has a protective effect on vascular and podocyte cell damage due to Ang-II. (?)The assessment of autophagic dynamics needs further studies.