Angiogenesis and Inflammation in Biological Barriers 3.0

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Immunology and Immunotherapy".

Deadline for manuscript submissions: closed (15 July 2023) | Viewed by 2875

Special Issue Editor

Special Issue Information

Dear Colleagues,

Owing to the success of our first and second Special Issues on angiogenesis and inflammation in biological barriers, I am pleased to announce the launch of a third volume. This Special Issue will gather publications that focus on two key processes, angiogenesis and inflammation, which strongly contribute to the functioning of highly vascularized biological barriers (BBs). The scope of this third Issue will be more focused on BB-associated pathologies. Biological barriers are essential for the integrity and proper functioning of many vertebrate organs, and are critical for the regulation of tissue homeostasis and protection against pathogens or other tissue-damaging agents. BBs separate internal and external compartments, and are formed by specialized cell types, such as epithelial and endothelial cells, that interface the body and the external environment. Recent studies have uncovered the role of new inflammatory and angiogenic proteins in the control of the integrity of these BBs and their physiological functioning. Deregulations in the expression and/or function of these proteins may explain BB-associated pathologies such as infections, exacerbated inflammation, tissue injury, and cancer. This Special Issue welcomes original research articles and reviews focused on pathological angiogenesis and inflammation in highly vascularized biological barriers.

Dr. Nadia Alfaidy
Guest Editor

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Keywords

  • biological barriers
  • inflammasome
  • angiogenesis
  • inflammation
  • vascularization
  • angiogenic factors
  • oxidative stress
  • cancer

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Published Papers (1 paper)

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Research

12 pages, 3860 KiB  
Article
Necroptosis Blockade Potentiates the Neuroprotective Effect of Hypothermia in Neonatal Hypoxic-Ischemic Encephalopathy
by Mathilde Chevin, Stéphane Chabrier, Marie-Julie Allard and Guillaume Sébire
Biomedicines 2022, 10(11), 2913; https://doi.org/10.3390/biomedicines10112913 - 13 Nov 2022
Cited by 3 | Viewed by 2546
Abstract
Neonatal encephalopathy (NE) caused by hypoxia-ischemia (HI) affects around 1 per 1000 term newborns and is the leading cause of acquired brain injury and neurodisability. Despite the use of hypothermia (HT) as a standard of care, the incidence of NE and its devastating [...] Read more.
Neonatal encephalopathy (NE) caused by hypoxia-ischemia (HI) affects around 1 per 1000 term newborns and is the leading cause of acquired brain injury and neurodisability. Despite the use of hypothermia (HT) as a standard of care, the incidence of NE and its devastating outcomes remains a major issue. Ongoing research surrounding add-on neuroprotective strategies against NE is important as HT effects are limited, leaving 50% of treated patients with neurological sequelae. Little is known about the interaction between necroptotic blockade and HT in neonatal HI. Using a preclinical Lewis rat model of term human NE induced by HI, we showed a neuroprotective effect of Necrostatin-1 (Nec-1: a compound blocking necroptosis) in combination with HT. The beneficial effect of Nec-1 added to HT against NE injuries was observed at the mechanistic level on both pMLKL and TNF-α, and at the anatomical level on brain volume loss visualized by magnetic resonance imaging (MRI). HT alone showed no effect on activated necroptotic effectors and did not preserve the brain MRI volume. This study opens new avenues of research to understand better the specific cell death mechanisms of brain injuries as well as the potential use of new therapeutics targeting the necroptosis pathway. Full article
(This article belongs to the Special Issue Angiogenesis and Inflammation in Biological Barriers 3.0)
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