NBR1-p62-Nrf2 mediates the anti-pulmonary fibrosis effects of protodioscin.

Background: Idiopathic pulmonary fibrosis is a persistent disease of the lung interstitium for which there is no efficacious pharmacological therapy. Protodioscin, a steroidal saponin, possesses diverse pharmacological properties; however, its function in pulmonary fibrosis is yet to be established. Hence, in this investigation, it was attempted to figure out the anti-pulmonary fibrosis influences of protodioscin and its pharmacological properties related to oxidative stress.

CPT1A as a potential therapeutic target for lipopolysaccharide-induced acute lung injury in mice.

Acute lung injury (ALI) remains a high mortality rate with dramatic lung inflammation and alveolar epithelial cell death. Although fatty acid β-oxidation (FAO) impairment has been implicated in the pathogenesis of ALI, whether Carnitine palmitoyltransferase 1A (CPT1A), the rate-limiting enzyme for FAO, plays roles in lipopolysaccharide (LPS)-induced ALI remains unclear. Accordingly, we focused on exploring the effect of CPT1A in the context of ALI and the underlying mechanisms.

Kindlin-2 protects pancreatic β cells through inhibiting NLRP3 inflammasome activation in diabetic mice.

Diabetes mellitus has been a major public health problem worldwide, characterized by insulin resistance and dysfunction of β-cells. A previous study showed that Kindlin-2 loss in β-cells dramatically reduces insulin secretion and decreases β-cell mass, resulting in severe diabetes-like phenotypes. It suggests that Kindlin-2 in β-cells play an important role in regulating glucose homeostasis.