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

Table 2

Autophagy modulation on apoptosis and aging in MSCs.

Experimental model	Molecular mechanisms	Autophagy effect on MSCs	References
Cecal ligation and puncture mouse model	Inflammatory microenvironment-induced autophagy inhibits the expression of the prosurvival gene Bcl-2 via suppressing reactive oxygen species/mitogen-activated protein kinase 1/3 pathway	Promotes apoptosis	[19]
Mice model	Activation of autophagy could reduce the adipogenic differentiation and promote proliferation of aged MSCs	Reverses aging	[107]
Mice model	Inhibition of autophagy could turn young MSCs into a relatively aged state by reducing their osteogenic differentiation and proliferation capacity and enhancing their adipogenic differentiation capacity	Promotes aging	[107]
Mice model	Impaired autophagy led to increased ROS and further induced the p16INK4a axis	Promotes aging	[108]
Cellular experiment	High glycemic treatment of MSCs increased ROS-mediated autophagy, leading to the formation of Beclin-1, Atg5, Atg7, Atg12, and LC3-II autophagosomes, which induced MSCs aging and local inflammation	Promotes aging	[109]