Table 2.
The protective effects of organelle-specific autophagy on various inflammatory diseases
Diseases | Multiple-organelle dysfunction | Quality control of multiple organelles by organelle-specific autophagy | Effects of organelle-specific autophagy | Refs |
---|---|---|---|---|
COPD | Dysfunction of mitochondria and severe disorganization of endoplasmic reticulum, Golgi, and lysosomes of lung fibroblasts | Induction of mitophagy | Improving survival of bronchial epithelial cells by removing damaged mitochondria and reducing production of ROS | [146] |
Restraining excessive inflammatory response in small airway epithelial cells by limiting inflammasome activation | ||||
Protecting against cellular senescence under CSE exposure | [147,149] | |||
Cardiovascular diseases | Dysfunction of mitochondria and uncontrolled ER stress | Induction of mitophagy | Maintaining homeostasis of cardiomyocytes | [150] |
Improving cardiomyopathy by limiting lethal inflammatory response | [151] | |||
Restraining cardiomyocyte loss and promoting tissue remodeling and fibrosis | [152] | |||
Protecting from hypertrophic cardiomyopathy by alleviating oxidative stress and insulin resistance | [153] | |||
Exerting cytoprotective effects under exposure to atherosclerosis | [154] | |||
Infectious diseases | Dysfunction of mitochondria and ER stress | Induction of mitophagy | Downregulating pro-inflammatory signals caused by S. aureus pneumonia | [157] |
Induction of reticulophagy | Limiting the replication of various viruses, including Zika, Dengue, and Ebola | [159,160] | ||
Maintaining cellular homeostasis under exposure to Gram-positive bacteria | [82] | |||
Induction of lysophagy | Inhibiting the invasion of intracellular M. tuberculosis | [98,99] | ||
Induction of nucleophagy | Maintaining integrity of epidermal barrier | [163] | ||
Sepsis | Damaged mitochondria, persistent ER stress, and aggregation of damaged peroxisomes | Induction of mitophagy | Protecting against cell death by eliminating damaged mitochondria | [166] |
Suppressing persistent NLRP3 inflammasome activation | [6] | |||
Induction of pexophagy | Restoring redox balance | [169] | ||
Neurodegenerative diseases | Dysfunction of mitochondria, impairment of RETREG1-mediated reticulophagy, aberrant response of peroxisomes, leakage of lysosomes, and failure of nucleophagy by mutation of LMNA | Induction of mitophagy | Maintaining viability of neurons by eliminating damaged mitochondria | [170,180] |
Improving familial and sporadic Parkinson diseases by decreasing accumulation of SNCA in the substantia nigra | [177,178] | |||
Restricting local inflammatory response | [179] | |||
Induction of reticulophagy | Essential for the survival of sensory and autonomic neurons | [79] | ||
Induction of pexophagy | Restoring function of peroxisomes and reducing ROS production | [113] | ||
Induction of nucleophagy | Delaying cell senescence and alleviating degenerative disorders | [195–197] |