The Role of Interaction between Mitochondria and the Extracellular Matrix in the Development of Idiopathic Pulmonary Fibrosis

Table 2

Properties of potential mitochondrial therapeutic agents in IPF treatment.

Potential therapeutic agents	Mechanism of action	Advantages	Disadvantages	Ref.
USP30 inhibitors	Mitophagy stimulation	Utilization of dysfunctioning of mitochondria	Excessive elimination of mitochondria	[26–28]
FGF-21 analogues	Oxidative stress inhibition	Decease ROS and ECM production	Unpredictable metabolic effects	[99, 104]
MitoQ	Increase mitochondrial respiration efficiency	Inhibition of oxidative stress, ROS production, and mitochondria dysfunction	High therapeutic dose	[102]
Sirtuin 3	Mitochondrial deacetylation level regulation	Inflammation suppression; Inhibition of oxidative stress; Apoptosis regulation; Autophagy regulation	Hiperautophagy; Apoptosis inhibition and cancerogenesis	[101]
STAT3 inhibitors	Induction of mitophagy	Utilization of malfunctioning mitochondria	Excessive elimination of mitochondria	[55]
Integrin’s blockers	Inhibition of latent TGF-β activation and mechanical stress transmission	Mitigate mechanical stress and TGF-β induced lung fibrosis	Crossactivity on inhibition integrin-ligand binding, integrin-mediated cell adhesion, and TGF-β signaling	[105]
SASP inhibitors	Inhibition of senescence-associated secretory phenotype (SASP) transition	The broad spectrum of antifibrotic action	Molecular targets with unpredictable effect	[75, 103]
PGC-1α analogs	Mitochondrial biogenesis stimulation	Increase mitochondria population	Increase ROS production	[28, 106]