SIRT4 regulates cellular communication network factor 2 expression through U2 small nuclear RNA auxiliary factor 2-mediated pre-mRNA splicing, presenting a potential therapeutic target for kidney fibrosis.

Genetic and chemical genetic analysis pinpoint defective epithelial cells as the driver for NPHP like phenotypes in Invs mutants, demonstrate genetic interaction between Invs and Ift88 and identify the HDAC inhibitor valproic acid as a suppressor for Invs mutant phenotypes.

The accumulation of SIRT4 in the nuclei of kidney cells drives kidney fibrosis, so blocking the movement of this protein could be a potential therapeutic strategy against fibrosis.

A meta-analysis of single-cell data reveals an advanced and conserved polarisation state of SPP1⁺ macrophages in multiple human fibrotic tissues.

Lymphangiogenic therapy VEGFCc156s improved angiotensin-II-induced impairments in heart function via novel mechanisms, which include transcriptional responses to alleviate inflammation and cardiac fibrosis, and systemic responses to ameliorate hypertension.

Fundc1-mediated mitophagy protects renal EPO-producing cells from myofibroblastic conversion under stresses.

Persistent Coxiella burnetii infected abdominal aorta aneurysms are associated with an immune-suppressed microenvironment.

Adult mouse fibroblasts maintain an embryonic gene expression signature, inherited from their organ of origin, that is important for organ homeostasis and fibrosis, and may assist in targeting fibrotic diseases in an organ-specific manner.

Potential commensalism between saprophytic and pathogenic Leptospira within a vertebrate host protects against severe leptospirosis and improves kidney homeostasis which helps Leptospira interrogans complete its enzootic cycle.

Adiponectin is an essential regulator for healthspan and is indispensable for sustaining a normal lifespan.