Kaempferol InhibitsP. intermediaLipopolysaccharide-Induced Production of Nitric Oxide Through Translational Regulation in Murine Macrophages: Critical Role of Heme Oxygenase-1-Mediated ROS Reduction

2013 ◽  
Vol 84 (4) ◽  
pp. 545-555 ◽  
Author(s):  
In Soon Choi ◽  
Eun-Young Choi ◽  
Ji-Young Jin ◽  
Hae Ryoun Park ◽  
Jeom-Il Choi ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Heme Oxygenase ◽  
Translational Regulation ◽  
Critical Role ◽  
Heme Oxygenase 1 ◽  
Murine Macrophages

scholarly journals A Dual Role of Heme Oxygenase-1 in Cancer Cells

2018 ◽  
Vol 20 (1) ◽  
pp. 39 ◽  
Author(s):  
Shih-Kai Chiang ◽  
Shuen-Ei Chen ◽  
Ling-Chu Chang
Keyword(s):  
Cell Death ◽  
Heme Oxygenase ◽  
Cancer Progression ◽  
Critical Role ◽  
Causative Factor ◽  
Protective Role ◽  
Dark Side ◽  
Heme Oxygenase 1 ◽  
Cellular Iron

Heme oxygenase (HO)-1 is known to metabolize heme into biliverdin/bilirubin, carbon monoxide, and ferrous iron, and it has been suggested to demonstrate cytoprotective effects against various stress-related conditions. HO-1 is commonly regarded as a survival molecule, exerting an important role in cancer progression and its inhibition is considered beneficial in a number of cancers. However, increasing studies have shown a dark side of HO-1, in which HO-1 acts as a critical mediator in ferroptosis induction and plays a causative factor for the progression of several diseases. Ferroptosis is a newly identified iron- and lipid peroxidation-dependent cell death. The critical role of HO-1 in heme metabolism makes it an important candidate to mediate protective or detrimental effects via ferroptosis induction. This review summarizes the current understanding on the regulatory mechanisms of HO-1 in ferroptosis. The amount of cellular iron and reactive oxygen species (ROS) is the determinative momentum for the role of HO-1, in which excessive cellular iron and ROS tend to enforce HO-1 from a protective role to a perpetrator. Despite the dark side that is related to cell death, there is a prospective application of HO-1 to mediate ferroptosis for cancer therapy as a chemotherapeutic strategy against tumors.

Critical Role of Endogenous Heme Oxygenase 1 as a Tuner of the Invasive Potential of Prostate Cancer Cells

2009 ◽  
Vol 7 (11) ◽  
pp. 1745-1755 ◽  
Author(s):  
Geraldine Gueron ◽  
Adriana De Siervi ◽  
Mercedes Ferrando ◽  
Marcelo Salierno ◽  
Paola De Luca ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Cells ◽  
Heme Oxygenase ◽  
Critical Role ◽  
Heme Oxygenase 1 ◽  
Prostate Cancer Cells ◽  
Invasive Potential

scholarly journals Targeting Heme Oxygenase-1 in Cardiovascular and Kidney Disease

Antioxidants ◽  
2019 ◽  
Vol 8 (6) ◽  
pp. 181 ◽  
Author(s):  
Heather A. Drummond ◽  
Zachary L. Mitchell ◽  
Nader G. Abraham ◽  
David E. Stec
Keyword(s):  
Blood Pressure ◽  
Cardiovascular System ◽  
Heme Oxygenase ◽  
Critical Role ◽  
Organ Injury ◽  
Renal Diseases ◽  
Heme Oxygenase 1 ◽  
Benefit Patient ◽  
Regulation Of Blood Pressure

Heme oxygenase (HO) plays an important role in the cardiovascular system. It is involved in many physiological and pathophysiological processes in all organs of the cardiovascular system. From the regulation of blood pressure and blood flow to the adaptive response to end-organ injury, HO plays a critical role in the ability of the cardiovascular system to respond and adapt to changes in homeostasis. There have been great advances in our understanding of the role of HO in the regulation of blood pressure and target organ injury in the last decade. Results from these studies demonstrate that targeting of the HO system could provide novel therapeutic opportunities for the treatment of several cardiovascular and renal diseases. The goal of this review is to highlight the important role of HO in the regulation of cardiovascular and renal function and protection from disease and to highlight areas in which targeting of the HO system needs to be translated to help benefit patient populations.

Heme oxygenase-1 induction improves ischemic renal failure: role of nitric oxide and peroxynitrite

2007 ◽  
Vol 293 (6) ◽  
pp. H3542-H3549 ◽  
Author(s):  
Miguel G. Salom ◽  
Susana Nieto Cerón ◽  
Francisca Rodriguez ◽  
Bernardo Lopez ◽  
Isabel Hernández ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Renal Failure ◽  
Acute Renal Failure ◽  
Heme Oxygenase ◽  
Heme Oxygenase 1 ◽  
Beneficial Effects ◽  
Medullary Blood Flow ◽  
Ischemic Renal Failure ◽  
Oxide Synthase

The present study evaluated the effects of heme oxygenase-1 (HO-1) induction on the changes in renal outer medullary nitric oxide (NO) and peroxynitrite levels during 45-min renal ischemia and 30-min reperfusion in anesthetized rats. Glomerular filtration rate (GFR), outer medullary blood flow (OMBF), HO and nitric oxide synthase (NOS) isoform expression, and renal low-molecular-weight thiols (–SH) were also determined. During ischemia significant increases in NO levels and peroxynitrite signal were observed (from 832.1 ± 129.3 to 2,928.6 ± 502.0 nM and from 3.8 ± 0.7 to 9.0 ± 1.6 nA before and during ischemia, respectively) that dropped to preischemic levels during reperfusion. OMBF and –SH significantly decreased after 30 min of reperfusion. Twenty-four hours later, an acute renal failure was observed (GFR 923.0 ± 66.0 and 253.6 ± 55.3 μl·min−1·g kidney wt−1 in sham-operated and ischemic kidneys, respectively; P < 0.05). The induction of HO-1 (CoCl2 60 mg/kg sc, 24 h before ischemia) decreased basal NO concentration (99.7 ± 41.0 nM), although endothelial and neuronal NOS expression were slightly increased. CoCl2 administration also blunted the ischemic increase in NO and peroxynitrite (maximum values of 1,315.6 ± 445.6 nM and 6.3 ± 0.5 nA, respectively; P < 0.05), preserving postischemic OMBF and GFR (686.4 ± 45.2 μl·min−1·g kidney wt−1). These beneficial effects of CoCl2 on ischemic acute renal failure seem to be due to HO-1 induction, because they were abolished by stannous mesoporphyrin, a HO inhibitor. In conclusion, HO-1 induction has a protective effect on ischemic renal failure that seems to be partially mediated by decreasing the excessive production of NO with the subsequent reduction in peroxynitrite formation observed during ischemia.

scholarly journals Critical Role of 5-Lipoxygenase and Heme Oxygenase-1 in Wound Healing

2014 ◽  
Vol 134 (5) ◽  
pp. 1436-1445 ◽  
Author(s):  
Ariane R. Brogliato ◽  
Andrea N. Moor ◽  
Shannon L. Kesl ◽  
Rafael F. Guilherme ◽  
Janaína L. Georgii ◽  
...  
Keyword(s):  
Wound Healing ◽  
Heme Oxygenase ◽  
Critical Role ◽  
Heme Oxygenase 1
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