RIPK4 promotes oxidative stress and ferroptotic death through the downregulation of ACSM1.

One of the most critical axes for cell fate determination is how cells respond to excessive reactive oxygen species (ROS)-oxidative stress. Extensive lipid peroxidation commits cells to death via a distinct cell death paradigm termed ferroptosis. However, the molecular mechanism regulating cellular fates to distinct ROS remains incompletely understood.

To target cellular senescence in diabetic kidney disease: the known and the unknown.

Cellular senescence represents a condition of irreversible cell cycle arrest, characterized by heightened senescence-associated beta-galactosidase (SA-β-Gal) activity, senescence-associated secretory phenotype (SASP), and activation of the DNA damage response (DDR). Diabetic kidney disease (DKD) is a significant contributor to end-stage renal disease (ESRD) globally, with ongoing unmet needs in terms of current treatments. The role of senescence in the pathogenesis of DKD has attracted substantial attention with evidence of premature senescence in this condition.

CGI1746 targets σR to modulate ferroptosis through mitochondria-associated membranes.

Ferroptosis is iron-dependent oxidative cell death. Labile iron and polyunsaturated fatty acid (PUFA)-containing lipids are two critical factors for ferroptosis execution. Many processes regulating iron homeostasis and lipid synthesis are critically involved in ferroptosis.

Renal histopathological lesions after liver transplantation: What can we find besides calcineurin inhibitor-induced nephrotoxicity?

Background: Chronic kidney disease (CKD) is a common complication after liver transplantation and is traditionally considered to be secondary to calcineurin inhibitors (CNIs). However, several studies have reported that the etiology of CKD after liver transplantation is broad and may only be assessed accurately by renal biopsy. The current study aimed to explore the usefulness of renal biopsies in managing CKD after liver transplantation in daily clinical practice.

STING controls energy stress-induced autophagy and energy metabolism via STX17.

The stimulator of interferon genes (STING) plays a critical role in innate immunity. Emerging evidence suggests that STING is important for DNA or cGAMP-induced non-canonical autophagy, which is independent of a large part of canonical autophagy machineries. Here, we report that, in the absence of STING, energy stress-induced autophagy is upregulated rather than downregulated.

Incremental diagnostic value of CMR-derived LA strain and strain rate in dialysis patients with HFpEF.

Objectives: To test whether left atrial (LA) strain and strain rate add incremental value in the diagnosis of heart failure with preserved ejection fraction (HFpEF) in dialysis patients over clinical and conventional parameters only.

Background: HFpEF frequently occurs in dialysis patients, however, the diagnosis of HFpEF is difficult. Although HFpEF is always companied with LA dysfunction, the performance of novel LA parameters, LA strain, and strain rate, in the diagnosis of HFpEF among dialysis patients remains unknown.

The predictive value of urinary kidney injury molecular-1 for long-term graft function in kidney transplant patients: a prospective study.

Background: Monitoring allograft function during the early stages is crucial, and therefore requires biomarkers more sensitive than serum creatinine (Scr). Kidney injury molecular-1 (KIM-1) is a potent biomarker; however, disparities exist in the literature concerning its predictive value in allograft function. Therefore, this study aimed to evaluate its predictive value for the long-term prognosis of kidney transplantation patients.

Texture Analysis of Native T1 Images as a Novel Method for Noninvasive Assessment of Uremic Cardiomyopathy.

Background: Noncontrast cardiac T times are increased in dialysis patients which might indicate fibrotic alterations in uremic cardiomyopathy.

Purpose: To explore the application of the texture analysis (TA) of T images in the assessment of myocardial alterations in dialysis patients.

Study Type: Case-control study.

Myocardial Iron Deficiency Quantification and Effective Cardiac Iron Management Strategy Exploration evaluated by Cardiac T2* Mapping in End-Stage Renal Disease Patients.

Purpose: To explore myocardial iron content using Cardiac T2* Mapping in dialysis patients undergoing oral iron therapy or intravenous iron supplements compared to healthy controls.

Methods: Fifty-nine dialysis patients, including 30 peritoneal dialysis (PD) patients who underwent oral iron therapy, 29 hemodialysis (HD) dialysis patients who underwent intravenous iron supplements, and 30 healthy controls were included in the study. Cardiac MRI, including cine, T2 stir, and T2* mapping, was conducted at 3.

Astragalus Polysaccharide Attenuates Cisplatin-Induced Acute Kidney Injury by Suppressing Oxidative Damage and Mitochondrial Dysfunction.

Cisplatin is a widely used chemotherapeutic drug in the treatment of various solid tumors. However, the cisplatin-induced acute kidney injury remains a disturbing complication, which still lacks effective prevention. Cisplatin-induced oxidative damage and mitochondrial dysfunction are anticipated to be crucial in the occurrence of kidney injury.