Nebivolol, a β1-adrenergic blocker, protects from peritoneal membrane damage induced during peritoneal dialysis

Liappas, Georgios; González-Mateo, Guadalupe; Aguirre, Anna Rita; Abensur, Hugo; Albar-Vizcaíno, Patricia; Parra, Emilio González; Sandoval, Pilar; Ramírez, Laura García; Peso, Gloria del; Acedo, Juan Manuel; Bajo, María Auxiliadora; Selgas, Rafael; Tomero, José Antonio Sánchez; López–Cabrera, Manuel; Aguilera, Abelardo

doi:10.18632/oncotarget.8780

Cited by 13 publications

(15 citation statements)

References 45 publications

(76 reference statements)

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“…Guba et al published that Rapamycin decreased the synthesis of VEGF by endothelial cells [111]. In vivo exposure to PDF in a mice model, significant reduction in VEGF in PD effluent and in the number of both peritoneal blood and lymph vessels was founded [41].…”

Section: Anti-angiogenic and Anti-lymphangiogenic Agentsmentioning

confidence: 99%

Pharmacological Preservation of Peritoneal Membrane in Peritoneal Dialysis

Gónzalez-Mateo¹,

Gallardo²,

AntonioSánchez-Tomero³

et al. 2016

Some Special Problems in Peritoneal Dialysis

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Peritoneal dialysis (PD) is an established renal replacement therapy for renal disease. It is based on the capacity of the peritoneum to act as a semipermeable membrane for the exchange of toxic solutes and water, which is called ultrafiltration capacity. Peritoneal membrane (PM) is lined by a monolayer of mesothelial cells (MCs), which lay on an extracellular matrix bed where other cell types and blood and lymphatic vessels can be found. Long-term exposure to hyperosmotic PD fluids (PDFs), peritonitis or hemoperitoneum causes peritoneal injury by the generation of an inflammatory state. Inflammatory cells and their mediators initiate a cascade of reactions promoting alterations in peritoneal cells, loss of MCs, fibrosis, vasculopathy, and angiogenesis, leading to ultrafiltration failure. Recent studies support that the so-called "mesothelial to mesenchymal transition" process of the MCs runs parallel to the anatomical and functional ridging of PM, which suggests that its inhibition might slow down or stop the PM damage. The fight against PM damage begins with the improvement in PDF biocompatibility. Complementary to this, an alternative approach to preserve the PM might be the use of pharmacological agents or molecular strategies. Here, we explain the existing research models for the development of new therapies and analyze several therapeutic options tested with them.

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Section: Anti-angiogenic and Anti-lymphangiogenic Agentsmentioning

confidence: 99%

Pharmacological Preservation of Peritoneal Membrane in Peritoneal Dialysis

Gónzalez-Mateo¹,

Gallardo²,

AntonioSánchez-Tomero³

et al. 2016

Some Special Problems in Peritoneal Dialysis

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“…Blocking β1-adrenergic receptor (β1-AR) expressed in peritoneal MCs is another therapeutic strategy to reduce angiogenesis induced during PD [129] since it has been observed that the block of this receptor is related with anti-angiogenic effects [152]. Indeed, the β1-AR antagonist Nebivolol has demonstrated to attenuate submesothelial vessel formation in a mice model of PD obtained by instillation of PDFs through a peritoneal catheter.…”

Section: Othersmentioning

confidence: 99%

“…Indeed, the β1-AR antagonist Nebivolol has demonstrated to attenuate submesothelial vessel formation in a mice model of PD obtained by instillation of PDFs through a peritoneal catheter. This effect may be associated with its direct interaction with the β1-AR, but it could also be due to the reduction of fibrosis and MMT [129].…”

Section: Othersmentioning

confidence: 99%

Angiogenesis and Lymphangiogenesis in Peritoneal Dialysis

Gónzalez-Mateo¹,

Pascual-Antón²,

Carrasco³

et al. 2018

Aspects in Dialysis

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The ultrafiltration failure during peritoneal dialysis (PD) is related to inflammatory responses induced by bio-incompatible PD fluids, which may lead to deterioration of peritoneal membrane (PM) function. Mesothelial cells, lymphocytes, macrophages and other cell types present in the peritoneal cavity are stimulated to produce cytokines and growth factors that promote pathological processes. Due to these factors, blood and lymphatic vessels proliferate and could be responsible for hyperfiltration and PM failure type III and IV. Vessels proliferation may be related to fibrosis, being the cause and/or effect of the mesenchymal conversion of different cell types such as mesothelial (MMT), bone marrow-derived (fibrocytes) or endothelial (vascular-and lymph-endo-MT) cells. Lymphangiogenesis in PD is a poorly analysed process; however, its contribution to peritoneal function disorders has been recently recognized. VEGF production is associated with blood and lymphatic vessels proliferation, while specifically lymphangiogenesis is mainly regulated by VEGF-C and VEGF-D. Excessive lymphatic fluid drainage from the abdominal cavity may be related with macromolecule and isosmotic solutions reuptake and convective reabsorption of solutes that were cleared from plasma by diffusion. Some drugs have been shown to modulate tissue fibrosis, MMT, EndoMT, angiogenesis and lymphangiogenesis and could represent interesting therapeutic strategies to protect the PM.

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“…74 A study in mouse model has suggested the role of beta-blocker nebivolol in preventing peritoneal dialysis induced fibrogenic responses. 75 Other drugs and agents which have been found to have some benefit in animal studies include rosiglitazone, N-acetyl cysteine, colchicine, angiotensin inhibition, thalidomide as well as biocompatible PD solutions. 60 However, the translation of these experimental evidence into clinical practice is awaited.…”

Section: Future Targetsmentioning

confidence: 99%

Abdominal cocoon: An enigmatic entity

Mandavdhare¹

2016

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Abdominal cocoon, variously described as encapsulating peritoneal sclerosis (EPS) or sclerosing encapsulating peritonitis or peritonitis chronica fibrosa incapsulata, represents a syndrome of clinical symptoms related to formation of a fibro-collagenous peritoneal membrane that involves the small intestinal loops. It is the outcome of several different etiologic processes. The major factors associated with development of an abdominal cocoon include continuous ambulatory peritoneal dialysis, tuberculosis, post-renal or liver transplant, use of beta-blockers although a proportion are of idiopathic origin. It is believed that the pathogenesis is driven by epithelial-to-mesenchymal transition of the mesothelial cells. The clinical presentation is related to development of altered gut motility resulting in abdominal pain and features of intestinal obstruction. Surgery is usually required in cases of unremitting intestinal obstruction. Although computed tomography may provide a pre-operative diagnosis, many cases are diagnosed at the time of surgery. Role of conservative therapy using drugs like steroids, tamoxifen, and mechanistic target of rapamycin (mTOR) inhibitors, or antitubercular therapy (in patients with tuberculosis) is uncertain. Early management aimed at the underlying etiological factor may ameliorate the symptoms and halt progression to formation of frank cocoon. Occasionally, conditions like peritoneal carcinomatosis or peritoneal encapsulation may mimic EPS.

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Nebivolol, a β1-adrenergic blocker, protects from peritoneal membrane damage induced during peritoneal dialysis

Cited by 13 publications

References 45 publications

Pharmacological Preservation of Peritoneal Membrane in Peritoneal Dialysis

Pharmacological Preservation of Peritoneal Membrane in Peritoneal Dialysis

Angiogenesis and Lymphangiogenesis in Peritoneal Dialysis

Abdominal cocoon: An enigmatic entity

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