Delayed administration of pituitary adenylate cyclase-activating polypeptide 38 ameliorates renal ischemia/reperfusion injury in mice by modulating Toll-like receptors

Khan, Altaf-M.; Li, Min; Abdulnour‐Nakhoul, Solange; Maderdrut, Jerome L.; Simon, Eric E.; Batuman, Vecihi

doi:10.1016/j.peptides.2012.09.023

Cited by 18 publications

(13 citation statements)

References 52 publications

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“…This is mainly because TLR4 can respond to angiotensin II, a DAMP, and cause subsequent vascular dysfunction and high blood pressure (Bomfim et al, 2015; Hernanz et al, 2015). Surprisingly, the evidence of TLR2 involved in hypertension is limited to inflammation in the renal system, where TLR2-activated NF-κB signaling is significantly correlated with renal ischemia/reperfusion injury (Khan et al, 2012). Recently, attentions have been drawn to TLR9 for its role in hypertension and blood pressure regulation.…”

Section: Toll-like Receptor Activation In Autoimmune and Inflammatorymentioning

confidence: 99%

Inhibition of Toll-Like Receptor Signaling as a Promising Therapy for Inflammatory Diseases: A Journey from Molecular to Nano Therapeutics

et al. 2017

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The recognition of invading pathogens and endogenous molecules from damaged tissues by toll-like receptors (TLRs) triggers protective self-defense mechanisms. However, excessive TLR activation disrupts the immune homeostasis by sustained pro-inflammatory cytokines and chemokines production and consequently contributes to the development of many inflammatory and autoimmune diseases, such as systemic lupus erythematosus (SLE), infection-associated sepsis, atherosclerosis, and asthma. Therefore, inhibitors/antagonists targeting TLR signals may be beneficial to treat these disorders. In this article, we first briefly summarize the pathophysiological role of TLRs in the inflammatory diseases. We then focus on reviewing the current knowledge in both preclinical and clinical studies of various TLR antagonists/inhibitors for the prevention and treatment of inflammatory diseases. These compounds range from conventional small molecules to therapeutic biologics and nanodevices. In particular, nanodevices are emerging as a new class of potent TLR inhibitors for their unique properties in desired bio-distribution, sustained circulation, and preferred pharmacodynamic and pharmacokinetic profiles. More interestingly, the inhibitory activity of these nanodevices can be regulated through precise nano-functionalization, making them the next generation therapeutics or “nano-drugs.” Although, significant efforts have been made in developing different kinds of new TLR inhibitors/antagonists, only limited numbers of them have undergone clinical trials, and none have been approved for clinical uses to date. Nevertheless, these findings and continuous studies of TLR inhibition highlight the pharmacological regulation of TLR signaling, especially on multiple TLR pathways, as future promising therapeutic strategy for various inflammatory and autoimmune diseases.

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Section: Toll-like Receptor Activation In Autoimmune and Inflammatorymentioning

confidence: 99%

Inhibition of Toll-Like Receptor Signaling as a Promising Therapy for Inflammatory Diseases: A Journey from Molecular to Nano Therapeutics

et al. 2017

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“…In endothelial cells, high-density lipoprotein from patients with chronic kidney disease activated TLR2 (independently of TLR1 and TLR6) and reduced nitric oxide bioavailability, leading to impaired endothelial repair, enhanced inflammation, and increased arterial pressure (Speer et al, 2013). In renal tubular epithelial cells, it was observed that TLR2 upregulated NACHT, leucine rich repeats, and PYD domains containing protein 3 inflammasome, as well as its substrate IL-1b (Kasimsetty et al, 2014), and TLR2-NF-kB signaling significantly contributed to renal ischemiareperfusion injury (Khan et al, 2012). Similarly, TLR5 has not been directly linked with hypertension, but it has been linked with metabolic syndrome, in which hypertension is one defining characteristic.…”

Section: B Hypertensionmentioning

confidence: 99%

Toll-like Receptors in the Vascular System: Sensing the Dangers Within

2015

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“…Blood urea nitrogen, serum creatinine, plasma and kidney homogenate TNF-α level were lower in PACAP-treated animals. Toll-like receptors, which are important mediators of innate immunity in the kidney, were also shown to participate in the protective effects of pacap [22,29].…”

Section: Effect Of Exogenous Pacap In Ischemia/reperfusion-induced Kimentioning

confidence: 99%

The effects of pituitary adenylate cyclase activating polypeptide in renal ischemia/reperfusion

László¹,

Kiss²,

Horváth³

et al. 2014

Acta Biologica Hungarica

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pituitary adenylate cyclase activating polypeptide (pacap) is a multifunctional neuropeptide occurring in the nervous system as well as in the peripheral organs. Beneficial action of PACAP has been shown in different pathological processes. The strong protective effects of the peptide are probably due to its complex modulatory actions in antiapoptotic, anti-inflammatory and antioxidant pathways. In the kidney, PACAP is protective in models of diabetic nephropathy, myeloma kidney injury, cisplatin-, gentamycinand cyclosporin-induced damages. Numerous studies have been published describing the protective effect of this peptide in renal ischemia/reperfusion. the present review focuses on the ischemia/reperfusioninduced kidney injury and gives a brief summary about the results published in this area.

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Delayed administration of pituitary adenylate cyclase-activating polypeptide 38 ameliorates renal ischemia/reperfusion injury in mice by modulating Toll-like receptors

Cited by 18 publications

References 52 publications

Inhibition of Toll-Like Receptor Signaling as a Promising Therapy for Inflammatory Diseases: A Journey from Molecular to Nano Therapeutics

Inhibition of Toll-Like Receptor Signaling as a Promising Therapy for Inflammatory Diseases: A Journey from Molecular to Nano Therapeutics

Toll-like Receptors in the Vascular System: Sensing the Dangers Within

The effects of pituitary adenylate cyclase activating polypeptide in renal ischemia/reperfusion

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