In response to ischemic, toxic or immunological insults, the more frequent injuries encountered by the kidney, cells must adapt to maintain vital metabolic functions and avoid cell death. Among the adaptive responses activated, autophagy emerges as an important integrator of various extracellular and intracellular triggers (often related to nutrients availability or immunological stimuli), which, as a consequence,may regulate cell viability, and also immune functions,both innate or adaptive. The aim of this review is to make the synthesis of the recent literature on the implications of autophagy in the kidney transplantation field and to discuss the future directions for research.
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http://dx.doi.org/10.1111/ajt.12533 | DOI Listing |
Biochem Biophys Rep
March 2025
Department of Cardiovascular Medicine, The First People's Hospital of Changzhou, The Third Affiliated Hospital of Soochow University, 213000, Changzhou, Jiangsu Province, China.
Background: Previous research has established that chronic kidney disease (CKD) and heart failure with preserved ejection fraction (HFpEF) often coexist. Although we have a preliminary understanding of the potential correlation between HFpEF and CKD, the underlying pathophysiological mechanisms remain unclear. This study aimed to elucidate the molecular mechanisms associated with CKD and HFpEF through bioinformatics analysis.
View Article and Find Full Text PDFCell Commun Signal
January 2025
Department of Cardiology, the 2nd Affiliated Hospital of Harbin Medical University, Harbin, 150001, China.
Oxidative stress-associated proximal tubular cells (PTCs) damage is an important pathogenesis of hypertensive renal injury. We previously reported the protective effect of VEGFR3 in salt-sensitive hypertension. However, the specific mechanism underlying the role of VEGFR3 in kidney during the overactivation of the renin-angiotensin-aldosterone system remains unclear.
View Article and Find Full Text PDFAging Cell
January 2025
Departamento de Genética y Biología Molecular, Centro de Investigación y de Estudios Avanzados, Ciudad de México, Mexico.
Hutchinson-Gilford progeria syndrome (HGPS) is a premature aging disease caused by progerin, a mutant variant of lamin A. Progerin anchors aberrantly to the nuclear envelope disrupting a plethora of cellular processes, which in turn elicits senescence. We previously showed that the chromosomal region maintenance 1 (CRM1)-driven nuclear export pathway is abnormally enhanced in patient-derived fibroblasts, due to overexpression of CRM1.
View Article and Find Full Text PDFPLoS One
January 2025
Department of Rheumatology, The Second Affiliated Hospital of Fujian Medical University, Quanzhou, P.R. China.
Introduction: Lupus nephritis (LN) is one of the most frequent and serious organic manifestations of systemic lupus erythematosus (SLE). Autophagy, a new form of programmed cell death, has been implicated in a variety of renal diseases, but the relationship between autophagy and LN remains unelucidated.
Methods: We analyzed differentially expressed genes (DEGs) in kidney tissues from 14 LN patients and 7 normal controls using the GSE112943 dataset.
Microb Pathog
January 2025
Department of Laboratory Medicine, Suzhou Mental Health Center, the Affiliated Guangji Hospital of Soochow University, Suzhou215137, Jiangsu, China.
Enterovirus 71 (EV-71) is a major pathogenic factor that causes hand, foot, and mouth disease in young children and infants. Given the limited treatments for EV-71 infection, discovering new host factors and understanding the mechanisms involved will aid in combating this viral infection. Neutral sphingomyelinase-2 (nSMase-2, encoded by SMPD3) is a crucial cellular cofactor in viral infection.
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