SPOP-mediated RIPK3 destabilization desensitizes LPS/sMAC/zVAD-induced necroptotic cell death.

RIPK1/RIPK3-MLKL signaling molecules are fundamental in initiating necroptotic cell death, but their roles in the development of colon cancer are unclear. This study reports that RIPK3 interacted with SPOP, a component of the E3 ligase within the Cul3 complex. This interaction leads to K48-linked ubiquitination and subsequent proteasomal degradation of RIPK3.

Niclosamide attenuates calcification in human heart valvular interstitial cells through inhibition of the AMPK/mTOR signaling pathway.

Calcific aortic valve disease (CAVD) is a considerable health burden with a lack of effective therapeutic options. There is an urgent need to develop interventions that inhibit the osteogenic transformation of valvular interstitial cells (VICs) and delay the calcification process. Niclosamide, an FDA-approved anti-helminthic drug, has emerged as a promising candidate that demonstrates a negative regulatory effect on porcine VICs calcification.

Mitogenomic Architecture of Atlantic Emperor (Actinopterygii: Spariformes): Insights into the Lineage Diversification in Atlantic Ocean.

The evolutionary history of emperors, particularly in the Atlantic and Indo-West Pacific Oceans, remains largely unmapped. This study explores the maternal lineage evolution of Lethrinids by examining the complete mitogenome of , which is endemic to the Eastern Atlantic Ocean. Utilizing advanced next-generation sequencing, we found that the mitogenome spans 16,789 base pairs and encompasses 37 genes, including 13 protein-coding genes (PCGs), two ribosomal RNAs, 22 transfer RNAs, and an AT-rich control region (CR).

Regenerative capacity of alveolar type 2 cells is proportionally reduced following disease progression in idiopathic pulmonary fibrosis-derived organoid cultures.

Background: Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive lung disease that leads to respiratory failure and death due to irreversible scarring of the distal lung. While historically considered a chronic inflammatory disorder, the aberrant function of the alveolar epithelium is now recognized to play a central role in IPF pathophysiology.

Purpose: This study aimed to investigate the regenerative capacity of AT2 cells using IPF-derived alveolar organoids and to examine the effects of disease progression on this capacity.