Different Levels of Autophagy Activity in Mesenchymal Stem Cells Are Involved in the Progression of Idiopathic Pulmonary Fibrosis

Table 1

Role of autophagy in the therapeutic potential of MSCs.

Disease model	Mechanism	Autophagy effect	Reference
Ischemic stroke	MSCs inhibit autophagy and promote cell survival by transferring miR-25 to support recovery of neurological function after stroke	Negative	[57]
Liver fibrosis	Autophagy inhibition via Becn1 downregulation improves the MSCs antifibrotic potential	Negative	[58]
Hypoxic-ischemic brain damage	MSCs reduce autophagy in hippocampal neurons partly through the AMPK/mTOR pathway	Negative	[59]
Osteoarthritis	MSCs enhance autophagy in chondrocytes via mTOR inhibition and protect articular cartilage from damage	Positive	[60]
Acute lung injury	MSCs enhance autophagy and ameliorate acute lung injury partially via delivery of miR-100	Positive	[61]
Idiopathic pulmonary fibrosis	Inhibition of miR-199a-5p enhances autophagy by regulating the Sirt1/AMPK signaling pathway and rejuvenates IPF-MSCs senescence	Positive	[62]
Parkinson’s disease	MSCs enhance autophagy and exert a neuroprotective effect through the modulation of α-synuclein	Positive	[63]
Alzheimer’s disease	MSCs enhance autophagy and increase β-amyloid clearance to improve neuronal survival against Aβ toxicity	Positive	[64]
Inflammatory bowel disease	Enhancement of autophagy in MSCs improves immunosuppression of MSCs by increasing Pacer levels	Positive	[65]
Diabetic kidney disease	MSCs diminish cell death in kidney tissue facing diabetic kidney disease, culminating in podocyte maintenance, and also downregulating the over induction of the autophagy pathway	A double-edged sword	[66]