Intracellular Organelles in Health and Kidney Disease Publisher Pubmed



Shamekhi Amiri F¹
Source: Nephrologie et Therapeutique Published:2019

Abstract

Subcellular organelles consist of smaller substructures called supramolecular assemblies and these in turn consist of macromolecules. Various subcellular organelles have critical functions that consist of genetic disorders of organelle biogenesis and several metabolic disturbances that occur during non-genetic diseases e.g. infection, intoxication and drug treatments. Mitochondrial damage can cause renal dysfunction as ischemic acute renal injury, chronic kidney disease progression. Moreover, mitochondrial dysfunction is an early event in aldosterone-induced podocyte injury and cardiovascular disease due to oxidative stress in chronic kidney disease. Elevated production of reactive oxygen species could be able to activate NLRP3 inflammasome representing new deregulated biological machinery and a novel therapeutic target in hemodialysis patients. Peroxisomes are actively involved in apoptosis and inflammation, innate immunity, aging and in the pathogenesis of age related diseases, such as diabetes mellitus and cancer. Peroxisomal catalase causes alterations of mitochondrial membrane proteins and stimulates generation of mitochondrial reactive oxygen species. High concentrations of hydrogen peroxide exacerbate organelles and cellular aging. The importance of proper peroxisomal function for the biosynthesis of bile acids has been firmly established. Endoplasmic reticulum stress-induced pathological diseases in kidney cause glomerular injury and tubulointerstitial injury. Furthermore, there is a link between oxidative stress and inflammations in pathological states are associated with endoplasmic reticulum stress. Proteinuria and hyperglycemia in diabetic nephropathy may induce endoplasmic reticulum stress in tubular cells of the kidney. Due to the accumulation in the proximal tubule lysosomes, impaired function of these organelles may be an important mechanism leading to proximal tubular toxicity. © 2018 Societe francophone de nephrologie, dialyse et transplantation