PKD1 (Polycystin 1)

P=N/A, N=30, Not yet recruiting, Loma Linda University | Trial completion date: Dec 2026 --> Apr 2027 | Trial primary completion date: Jul 2026 --> Dec 2026

These findings highlight PKD isoforms as potential therapeutic targets, particularly in cancer settings where metabolic dysfunction plays a contributing role. While current PKD inhibitors lack isoform specificity, future therapeutic strategies focused on PKD2 and PKD3 modulation may offer selective control over invasion, immune evasion, and metabolic reprogramming in metabolically comorbid cancer patients.

Loss of Snhg5 did not attenuate cyst formation; if anything, disease severity was mildly but not significantly exacerbated. These findings indicate that Snhg5 modulates cell-cycle control and is dispensable for kidney development and cystogenesis in collecting duct-derived cysts.

Third, it integrates translational insights rarely synthesized in prior work: mapping natural compounds (icariin II and artesunate), repurposed drugs (sorafenib and melatonin), and novel modulators to disease stages (e.g., Lip-1 for fibrosis and salinomycin for RCC stem cells); highlighting strategies to reverse ferroptosis-related drug resistance (targeting DPP9 in RCC); and identifying ferroptosis-related genes (ACSL4 and PDIA4) as prognostic biomarkers. This review not only synthesizes ferroptosis pathophysiology and research advances but also delineates disease-tailored therapeutic strategies. By addressing key knowledge gaps-crosstalk between ferroptosis and other cell death modalities (e.g., pyroptosis), lack of kidney-specific clinical biomarkers, and underexplored roles in autoimmune nephritides-it provides a conceptual roadmap for mechanism-based diagnostics, precision therapeutics, and rational drug combinations, transcending traditional disease boundaries to advance clinical translation for both primary and secondary kidney diseases.

Overall, CBX8 phosphorylation by PKD1 impaired PRC1 complex integrity and activity, mitigated H2AK119ub1 level, caused the upregulation of multiple target genes repressed by CBX8, and decreased CBX8, H2AK119ub1, and H3K27me3 enrichment at INK4A/ARF locus, thereby derepressing p16INK4A and facilitating cellular senescence. Collectively, these results suggest that PKD1-mediated CBX8 phosphorylation at T234 and S256/311 is a key mechanism governing CBX8 function, including cell senescence.

A genotype-first ascertainment of individuals in genomic research allows for a more comprehensive assessment of Mendelian disease and removes biases that confound our understanding of the penetrance and presentation of these conditions.

This article aims to review the most recent literature on the diagnosis and management of renal lesions in tuberous sclerosis complex (TSC), with a particular focus on the role of various imaging techniques. Given the multifactorial nature of this disease, this review emphasizes the importance of a multidisciplinary approach, including various imaging methods, to improve the care and treatment outcomes of children with tuberous sclerosis complex.

Renal hemorrhage was presumed to result from vascular disruption and rupture of the internal elastic lamina because of cyst and AML progression. The combination of extensive renal cyst formation related to PKD1 deletion and AML lesions corresponding to TSC2 deletion may contribute to the rapid progression of kidney dysfunction in patients with PKDTS.

P4, N=80, Completed, China-Japan Friendship Hospital; China-Japan Friendship Hospital

We delineate implications of arteriolar angiogenesis in cancer stem cell development and anti-angiogenic immunotherapeutic strategies, highlighting anti-angiogenic strategy in combination with immune checkpoint blockade in pancreatic cancers. In summary, this review article seeks to develop the concept of arteriolar angiogenesis and yield insights into developing novel vascular targeting and immune therapies to cure cancers and cardiovascular and neurovascular diseases manifested with abnormal angiogenesis.