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Endothelial Cell Metabolism under Pathological Conditions

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Dear Colleagues,

The vasculature represents a truly remarkable organ that covers multiple physiological functions, including the supply of nutrients and oxygen, maintenance of pH and temperature, waste removal, and immune surveillance. By virtue of their localization, endothelial cells (ECs), lining the inner side of blood vessels, are directly exposed to blood metabolites and nutrients and pose as frontline regulators of systemic deregulations.

When blood vessels go awry, abnormal/dysfunctional ECs undergo behavioral plasticity and (metabolic) reprogramming, which can promote life-threatening diseases, including cancer, hypertension, stroke, diabetes, and atherosclerosis. On the flip side, pathogen infections also induce vessel dyshomeostasis that participates in the pathogenesis of several disorders with the vasculature as a central player.

Over the past decade, endothelial metabolism has been under the spotlight of intensive investigations, and a flurry of studies on EC metabolism has unraveled pathological metabolic abnormalities that can be therapeutically targeted. Recently, with the advent of state-of-the-art technologies allowing the analysis of cell heterogeneity, metabolic crosstalk studies and therapeutic considerations to target EC metabolic rewiring are required.

This Special Issue welcomes the submission of original research articles, meta-analyses, and reviews that help characterize endothelial metabolic aspects related to pathological disorders.

Dr. Lucas Treps
Guest Editor

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Keywords

endothelial cell metabolism
cancer
atherosclerosis
diabetes
hypertension
cardiovascular diseases
inflammation
infection

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Research

14 pages, 12936 KiB

Open AccessArticle

Targeting Endothelial Cell Metabolism by Inhibition of Pyruvate Dehydrogenase Kinase and Glutaminase-1

by Céline A. Schoonjans, Barbara Mathieu, Nicolas Joudiou, Luca X. Zampieri, Davide Brusa, Pierre Sonveaux, Olivier Feron and Bernard Gallez

J. Clin. Med. 2020, 9(10), 3308; https://doi.org/10.3390/jcm9103308 - 15 Oct 2020

Cited by 13 | Viewed by 3200

Abstract

Targeting endothelial cell (EC) metabolism should impair angiogenesis, regardless of how many angiogenic signals are present. The dependency of proliferating ECs on glucose and glutamine for energy and biomass production opens new opportunities for anti-angiogenic therapy in cancer. The aim of the present study was to investigate the role of pyruvate dehydrogenase kinase (PDK) inhibition with dichloroacetate (DCA), alone or in combination with the glutaminase-1 (GLS-1) inhibitor, Bis-2-(5-phenylacetamido-1,3,4-thiadiazol-2-yl) ethyl sulfide (BPTES), on Human umbilical vein endothelial cells (HUVECs) metabolism, proliferation, apoptosis, migration, and vessel formation. We demonstrated that both drugs normalize HUVECs metabolism by decreasing glycolysis for DCA and by reducing glutamate production for BPTES. DCA and BPTES reduced HUVECs proliferation and migration but have no impact on tube formation. While DCA increased HUVECs respiration, BPTES decreased it. Using both drugs in combination further reduced HUVECs proliferation while normalizing respiration and apoptosis induction. Overall, we demonstrated that DCA, a metabolic drug under study to target cancer cells metabolism, also affects tumor angiogenesis. Combining DCA and BPTES may reduce adverse effect of each drug alone and favor tumor angiogenesis normalization. Full article

(This article belongs to the Special Issue Endothelial Cell Metabolism under Pathological Conditions)

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13 pages, 1105 KiB

Open AccessArticle

The Vascular Side of Chronic Bed Rest: When a Therapeutic Approach Becomes Deleterious

by Anna Pedrinolla, Alessandro L. Colosio, Roberta Magliozzi, Elisa Danese, Emine Kirmizi, Stefania Rossi, Silvia Pogliaghi, Massimiliano Calabrese, Matteo Gelati, Ettore Muti, Emiliano Cè, Stefano Longo, Fabio Esposito, Giuseppe Lippi, Federico Schena and Massimo Venturelli

J. Clin. Med. 2020, 9(4), 918; https://doi.org/10.3390/jcm9040918 - 27 Mar 2020

Cited by 13 | Viewed by 2879

Abstract

The interplay between chronic constraint and advanced aging on blood flow, shear-rate, vascular function, nitric oxide (NO)-bioavailability, microcirculation, and vascular inflammation factors is still a matter of debate. Ninety-eight individuals (Young, n = 28, 23 ± 3 yrs; Old, n = 36, 85 ± 7 yrs; Bedridden, n = 34, 88 ± 6 yrs) were included in the study. The bedridden group included old individuals chronically confined to bed (3.8 ± 2.3 yrs). A blood sample was collected and analyzed for plasma nitrate, and vascular inflammatory markers. Hyperemic response (∆peak) during the single passive leg movement (sPLM) test was used to measure vascular function. Skeletal muscle total hemoglobin was measured at the vastus lateralis during the sPLM test, by means of near infrared spectroscopy (NIRS). Bedridden subjects revealed a depletion of plasma nitrates compared with Old (−23.8%) and Young (−31.1%). Blood flow was lower in the Bedridden in comparison to Old (−20.1%) and Young (−31.7%). Bedridden presented lower sPLM ∆peak compared Old (−72.5%) and the Young (−83.3%). ∆peak of NIRS total hemoglobin was lower in the Bedridden compared to that in the Young (−133%). All vascular inflammatory markers except IL-6 were significantly worse in the Bedridden compared to Old and Young. No differences were found between the Old and Young in inflammatory markers. Results of this study confirm that chronic physical constraint induces an exacerbation of vascular disfunction and differential regulation of vascular-related inflammatory markers. The mechanisms involved in these negative adaptations seems to be associated with endothelial dysfunction and consequent diminished NO-bioavailability likely caused by the reduced shear-rate consequential to long-term reduction of physical activity. Full article

(This article belongs to the Special Issue Endothelial Cell Metabolism under Pathological Conditions)

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