Ischemic kidney injury and mechanisms of tissue repair

Sabbahy, Marwa El; Vaidya, Vishal S.

doi:10.1002/wsbm.133

Cited by 93 publications

(83 citation statements)

References 81 publications

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“…To address this fea sibility, we conducted studies in mice cells, leukocytes, and renal parenchymal cells (7)(8)(9)(10)(11). Particularly, interplay bet ween inflammatory cytokines/chemo kines, apoptotic factors and reactive oxygen species (ROS) has been observed during the course of IRinduced renal injury (12)(13)(14)(15). Because of this complex ity, its underlying molecular mechanisms remained poorly understood (16,17).…”

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confidence: 99%

Aloperine Protects Mice against Ischemia-Reperfusion (IR)-Induced Renal Injury by Regulating PI3K/AKT/mTOR Signaling and AP-1 Activity

Zhang

et al. 2015

Mol Med

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Aloperine is a quinolizidine alkaloid extracted from the leaves of Sophora plants. It has been recognized with the potential to treat inflammatory and allergic diseases as well as tumors. In this report, we demonstrate that pretreatment with aloperine provided protection for mice against ischemia-reperfusion (IR)-induced acute renal injury as manifested by the attenuated inflammatory infiltration, reduced tubular apoptosis, and well-preserved renal function. Mechanistic studies revealed that aloperine selectively repressed IL-1β and IFN-γ expression by regulating PI3K/Akt/mTOR signaling and NF-κB transcriptional activity. However, aloperine did not show a perceptible impact on IL-6 and TGF-β expression and the related Jak2/Stat3 signaling. It was also noted that aloperine regulates AP-1 activity, through which it not only enhances SOD expression to increase reactive oxygen species (ROS) detoxification but also promotes the expression of antiapoptotic Bcl-2, thereby preventing tubular cells from IR-induced apoptosis. Collectively, our data suggest that administration of aloperine prior to IR insults, such as renal transplantation, could be a viable approach to prevent IR-induced injuries.

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confidence: 99%

Aloperine Protects Mice against Ischemia-Reperfusion (IR)-Induced Renal Injury by Regulating PI3K/AKT/mTOR Signaling and AP-1 Activity

Zhang

et al. 2015

Mol Med

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“…Recovery from ischemic and nephrotoxic AKI depends on regeneration of damaged tubular cells. Renal stem or progenitor cells outside the nephron migrate into the damaged nephrons and then regenerate the tubules (1,2). Several studies suggest that there is a very delicate and dynamic relationship between tissue repair and progression or regression of renal injury (2).…”

Section: öZmentioning

confidence: 99%

“…Renal stem or progenitor cells outside the nephron migrate into the damaged nephrons and then regenerate the tubules (1,2). Several studies suggest that there is a very delicate and dynamic relationship between tissue repair and progression or regression of renal injury (2). A number of renal tissue derived growth factors such as hepatocyte growth factor (HGF) and insulin-like growth factor 1 (IGF-1), which act as autocrine or paracrine regulators, are involved in the repair process.…”

Section: öZmentioning

confidence: 99%

“…Incomplete recovery may result in chronic and end-stage renal disease. Some growth factors, cell cycle and anti-apoptotic factors, and renal progenitor cells are included in this process (2). Epidermal growth factor (EGF), hepatocyte growth factor (HGF), and insulin-like growth factor I (IGF-1), administered to animals subjected to renal ischemia, reduce the extent of renal dysfunction and accelerate the recovery of the kidney (6, 7).…”

Section: Dıscussıonmentioning

confidence: 99%

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Hypothyroidism as an Obstacle to the Resolution of Acute Kidney Injury

Yıldız¹,

Oruç²,

Gül³

et al. 2016

Turk Neph Dial Transpl

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We described the clinical course of 4 patients with acute kidney injury (AKI) in whom kidney function improvement was delayed because of concomitant hypothyroidism. After initiating thyroid hormone replacement therapy, the kidney function improved partially or completely. We discussed the underlying possible pathophysiological mechanisms of delayed recovery. A 33-year-old female presented with kidney failure following severe preeclampsia. She was diagnosed with hypothyroidism. The second case was a 70-year-old male who was healthy previously, and presented with elevated serum creatinine. The third patient was a 72-year-old female, who was admitted with non-oliguric AKI associated with aminoglycoside and non-steroid anti-inflammatory drug exposure. The fourth patient was a 60-yearold female under amiodarone treatment after coronary bypass grafting who presented with fatigue, and AKI. We suggest that delayed recovery of kidney dysfunction might be associated with hypothyroidism that prevents regeneration of tubular cells. KEY wORdS: Acute kidney injury, Hypothyroidism, Thyroid hormone replacement therapy ÖzAkut böbrek hasarının (ABH) mortalite ve morbiditesi yüksektir. Eşlik eden sistemik hastalık varlığında iyileşmesi zorlaşır ve gecikir. Hipotiroidi, tanı konulmadığı ve tedavi edilmediği durumda ABH iyileşmesini engelleyebilir. Eşlik eden hipotiroidi nedeni ile iyileşmesi geciken 4 ABH olgusunu takdim ettik. İlk olgu olan, ciddi pre-eklampsi sonrası ABH gelişen 33 yaşındaki kadın hastada hipotiroidi tespit edildi. İkinci olgu hiçbir sistemik hastalığı olmayan 70 yaşında bir erkek, diğeri ise aminoglikozid ve non-steroid anti inflamatuvar ilaç kullanımına bağlı non-oligürik ABH gelişen 72 yaşında kadın hastaydı. Son olgu ise koroner bypass operasyonu sonrası amiodaron tedavisi altında ABH ile başvuran 60 yaşında kadın hastaydı. Tüm hastalarda, eşlik eden hipotiroidi tespit edildi. Tiroid hormon replasman tedavisi başlandı ve sonrasında ABH tam ya da kısmi olarak iyileşti. Yazımızda ABH iyileşmesinin gecikmesinde hipotiroidi ile ilişkili olabilecek patofizyolojik mekanizmalar tartışıldı. Hipotiroidism, tübüler hücrelerin rejenerasyonunu engelleyerek böbrek fonksiyonlarının iyileşmesinin gecikmesine neden olabilir. Ayrıca tedavi edilmediği durumlarda ABH iyileşmesini engelleyebilir.

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“…In recent years, acute renal injury (AKI) has accounted for 67.2% of the multi-organ injuries caused by global emergencies and natural disasters. To detect renal injury earlier and treat it in time, the international medical community has increasingly referred to the term AKI (El Sabbahy and Vaidya, 2011). The etiologies of AKI are various, with complex mechanisms, among which ischemia and toxins are the 2 main causes.…”

Section: Introductionmentioning

confidence: 99%

In vivo mechanism study of NGAL in rat renal ischemia-reperfusion injury

Zang

Zhang

et al. 2014

Genet. Mol. Res.

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ABSTRACT. This study aimed to determine the protective effect and mechanism of neutrophil gelatinase-associated lipocalin (NGAL) in rat kidney on ischemia/reperfusion injury (I/R). The rat I/R model was set up by cutting one kidney and clamping the contralateral renal pedicle for 45 min. Male SD rats were randomly divided into sham-operation, I/R and NGAL groups. Hematoxylin-eosin staining was performed to observe the renal pathological changes in the 3 groups; serum creatinine (Scr) and blood urea nitrogen (BUN) determined in blood samples taken from the inferior vena cava 24 h after the reperfusion were measured; TUNEL was used to observe the apoptosis of renal tubular epithelial cells; immunohistochemistry was performed to evaluate the expressions of Bax and activated caspase-3; Western blotting was used to determine the expression changes in apoptotic proteins Fas and Bcl-2. Compared with the I/R group, Scr and BUN of the NGAL group were 63.400 ± 11.908 vs 121.857 ± 17.151 µM and 14.840 ± 2.868 vs 28.557 ± 6.434 mM, respectively. The number of apoptotic tubular epithelial cells was reduced (7.800 ± 1.924 vs 15.400 ± 3.049); the expression of 8741 ©FUNPEC-RP www.funpecrp.com.br Genetics and Molecular Research 13 (4): 8740-8748 (2014) Study of NGAL in renal ischemia-reperfusion injury renal tissue Fas mRNA of the NGAL group was decreased (2.34 ± 0.51 vs 6.84 ± 2.34); the expression of the Bax protein was lower (7.440 ± 1.640 vs 15.456 ± 1.955%); the expression of the CC3 protein was decreased (3.171 ± 0.321 vs 7.291 ± 1.059%), while the expression of the Bcl-2 protein increased (6.91 ± 1.64 vs 5.30 ± 1.48), P < 0.05. NGAL had a protective effect towards the renal tubular epithelial cells in I/R, and the effect might have been associated with the reduction in apoptosis and the altered expression of apoptotic proteins, which would thereby reduce tissue damage and protect the kidney.

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Ischemic kidney injury and mechanisms of tissue repair

Cited by 93 publications

References 81 publications

Aloperine Protects Mice against Ischemia-Reperfusion (IR)-Induced Renal Injury by Regulating PI3K/AKT/mTOR Signaling and AP-1 Activity

Aloperine Protects Mice against Ischemia-Reperfusion (IR)-Induced Renal Injury by Regulating PI3K/AKT/mTOR Signaling and AP-1 Activity

Hypothyroidism as an Obstacle to the Resolution of Acute Kidney Injury

In vivo mechanism study of NGAL in rat renal ischemia-reperfusion injury

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