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Potential of Fenugreek in Management of Kidney and Lung Disorders
Published in Dilip Ghosh, Prasad Thakurdesai, Fenugreek, 2022
Amit D. Kandhare, Anwesha A. Mukherjee-Kandhare, Subhash L. Bodhankar
A study demonstrated the potential of dietary fenugreek seed (3%) administration against renin-angiotensin system-mediated renal damage in diabetic rats (Pradeep, Barman, and Srinivasan 2019). Fenugreek seed administration showed profound down-regulation in renal glucose transporters (GLUT-1 and GLUT-2), renal angiotensin-converting enzyme (ACE activity) and AT1 receptor expression, metabolites of the polyol pathway, and N-acetyl-β-d-glycosaminidase activity. The upregulated expression of kidney injury molecule-1, inducible nitric oxide, and type I collagen were markedly ameliorated by dietary fenugreek. Furthermore, podocyte damage was partially restored by fenugreek administration reflected by a correction in urinary nephrin, podocin, and podocalyxin markers. Diabetes-induced renal aberrations were also reduced by dietary fenugreek intake. The researcher concluded that dietary intake of fiber-rich fenugreek seeds was associated with inhibition of glucose translocation and renin-angiotensin system, which halted the development of diabetic nephropathy (Pradeep, Barman, and Srinivasan 2019).
Renal system
Published in Pankaj Desai, Pre-eclampsia, 2020
Two more lesions that have been described in the kidneys of patients affected by pre-eclampsia are focal segmental glomerular sclerosis (FSGS) and its variants described as early cellular lesions or glomerular tip lesions. The clinical bearing of these lesions is unknown, and therefore, they remain by and large confined to the realms of pathology books of the disease. Podocyte loss is the fundamental basis of glomerulosclerosis. FSGS is a progressive glomerular disease, and its glomerular features are a prototype of podocyte loss-driven glomerulosclerosis. The glomerular pathology of FSGS is characterised by a focal and segmental location of the sclerotic lesions in human FSGS; segmental sclerosis often shows simultaneous intra- and extra-capillary changes, including parietal cell migration, capillary collapse, hyaline deposition, intra-capillary thrombi and occasional hypercellularity. This suggests that local cellular events, initiated by podocyte loss, are the basis of the segmental lesions in FSGS.15
Familial Wilms Tumor and Related Syndromes
Published in Dongyou Liu, Handbook of Tumor Syndromes, 2020
The kidneys are a pair of bean-shaped organs (of 10–12 cm in length, 5–7 cm in width, 2–3 cm in thickness, and 135–150 g in weight) that are located along the posterior muscular wall of the abdominal cavity. Covered by a thin layer of fibrous connective tissue (the renal capsule), the kidneys comprise an outlayer of soft, dense, vascular renal cortex, and an inner renal medulla, the latter of which is composed of seven cone-shaped renal pyramids separated by the cortical tissue (called renal columns of Bertin). Each kidney contains around 1 million individual nephrons (the functional units), which are made of renal corpuscle and renal tubule. The renal corpuscle comprises the capillaries of the glomerulus that is surrounded by the glomerular capsule (or Bowman's capsule, a cup-shaped double layer of simple squamous epithelium with a hollow space between the layers). The glomerulus consists of podocytes and a basement membrane allowing water and certain solutes to be filtered across. Podocytes form a thin filter with the endothelium of the capillaries to separate urine from blood passing through the glomerulus. The outer layer of the glomerular capsule keeps the urine separated from the blood within the capsule. At the far end of the glomerular capsule is the mouth of the renal tubule, which carries urine from the glomerular capsule to the renal pelvis.
Combination therapy with DHA and BMSCs suppressed podocyte injury and attenuated renal fibrosis by modulating the TGF-β1/Smad pathway in MN mice
Published in Renal Failure, 2023
Yongzhang Li, Suzhi Chen, Jinchuan Tan, Yan Zhou, Meifang Ren, Qian Zhang, Meijiao Zhao, Guodong Yuan, Wenxi Zhang, Fengwen Yang
Podocytes are terminally differentiated cells in the glomerulus with regularly spaced foot processes that control glomerular filtration via the slit diaphragm [30]. Persistent podocyte injury results in podocyte loss and death, leading to progressive kidney damage and ultimately kidney failure [31]. Indeed, podocyte injury enhanced the increase in proteinuria; as a result, podocytes are believed to be the primary target of MN. Podocin and nephrin are the main components of the slit diaphragm, which play key roles in maintaining filtration barrier integrity [32]. In the present study, we found that combination therapy with DHA and BMSCs decreased the expression of podocin and nephrin. These results suggested that combination therapy with DHA and BMSCs has the potential to protect podocytes during kidney injury.
Progress in understanding primary glomerular disease: insights from urinary proteomics and in-depth analyses of potential biomarkers based on bioinformatics
Published in Critical Reviews in Clinical Laboratory Sciences, 2023
Lili Ge, Jianhua Liu, Baoxu Lin, Xiaosong Qin
As these collective findings highlight, potential IgAN biomarkers are related mainly to podocytes, immune complexes, and complement components. Podocytes, together with basement membrane and capillary endothelial cells, constitute the glomerular hemofiltration barrier and are one of the main cell types that maintain normal structure and function of the glomerular hemofiltration membrane. When podocytes are damaged, symptoms such as proteinuria occur. IgAN is an autoimmune disease. Galactose-deficient IgA1 exposes its hinge region epitopes, resulting in the production of IgA antibodies against abnormal IgA1, along with the formation and deposition of immune complexes in the mesangial region. IgA deposited in the mesangial region can activate the complement system through the bypass pathway and mannose-binding lectin pathway, which promotes inflammation and further pathological injury. Therefore, the level of complement components in urine may be closely related to the disease.
LncRNA XIST protects podocyte from high glucose-induced cell injury in diabetic nephropathy by sponging miR-30 and regulating AVEN expression
Published in Archives of Physiology and Biochemistry, 2023
Bendan Long, Yun Wan, Siqin Zhang, Lisa Lv
It is acknowledged that podocytes play a crucial role in the development of DN. Podocytes are specialised glomerular epithelial cells that form a layer of the filtration barrier in the kidney, which is terminally differentiated with limited capacity to renew. In animal models, podocyte injury and loss occur early during diabetes (Susztak et al. 2004). The identification of early metabolic changes in podocytes is thought to be critical for understanding the pathogenesis of diabetic kidney disease (Reidy et al. 2014). Thus, it is of great importance to determine the prognosis of DN. Podocyte foot processes are interconnected by slit diaphragms and form the final filtration barrier (Chen et al. 2017). It was reported that the reduction in podocytes number mediated by apoptosis was observed in patients with both early and late DN as well as in the animal DN models (Susztak et al. 2006, Tung et al. 2018). Increasing evidence has indicated that podocyte apoptosis coincides with albuminuria onset and precedes podocytopenia in different mouse models of diabetes (Gu et al. 2016, Huang et al. 2017). Thus, targeting podocytes could be a promising strategy for the treatment of DN.