Genetic counselling and prenatal diagnosis in disorders of the mitochondrial energy metabolism

1996 ◽  
Vol 19 (4) ◽  
pp. 581-587 ◽  
Author(s):  
W. Ruitenbeek ◽  
U. Wendel ◽  
B. C. J. Hamel ◽  
J. M. F. Trijbels
Keyword(s):  
Prenatal Diagnosis ◽  
Energy Metabolism ◽  
Genetic Counselling ◽  
Mitochondrial Energy Metabolism

Therapeutic Approaches Using Riboflavin in Mitochondrial Energy Metabolism Disorders

2016 ◽  
Vol 17 (13) ◽  
pp. 1527-1534 ◽  
Author(s):  
Bárbara J. Henriques ◽  
Tânia G. Lucas ◽  
Cláudio M. Gomes
Keyword(s):  
Energy Metabolism ◽  
Therapeutic Approaches ◽  
Mitochondrial Energy Metabolism

Mitochondrial energy metabolism is negatively regulated by cannabinoid receptor 1 in intact human epidermis

2020 ◽  
Vol 29 (7) ◽  
pp. 616-622 ◽  
Author(s):  
Attila Oláh ◽  
Majid Alam ◽  
Jérémy Chéret ◽  
Nikolett Gréta Kis ◽  
Zoltán Hegyi ◽  
...  
Keyword(s):  
Energy Metabolism ◽  
Cannabinoid Receptor ◽  
Human Epidermis ◽  
Cannabinoid Receptor 1 ◽  
Mitochondrial Energy Metabolism

scholarly journals Mitochondrial P2X7 receptor localization modulates energy metabolism enhancing physical performance

Function ◽  
2021 ◽  
Author(s):  
Alba Clara Sarti ◽  
Valentina Vultaggio-Poma ◽  
Simonetta Falzoni ◽  
Sonia Missiroli ◽  
Anna Lisa Giuliani ◽  
...  
Keyword(s):  
Energy Metabolism ◽  
Physical Fitness ◽  
P2x7 Receptor ◽  
Human Fibroblasts ◽  
Atp Synthesis ◽  
Heart Tissue ◽  
Mitochondrial Potential ◽  
Mitochondrial Energy Metabolism ◽  
Microglia Cell ◽  
Basal Expression

Abstract Basal expression of the P2X7 receptor (P2X7R) improves mitochondrial metabolism, ATP synthesis and overall fitness of immune and non-immune cells. We investigated P2X7R contribution to energy metabolism and subcellular localization in fibroblasts (mouse embryo fibroblasts and HEK293 human fibroblasts), mouse microglia (primary brain microglia and the N13 microglia cell line), and heart tissue. The P2X7R localizes to mitochondria, and its lack a) decreases basal respiratory rate, ATP-coupled respiration, maximal uncoupled respiration, resting mitochondrial potential, mitochondrial matrix Ca2+ level, b) modifies expression pattern of oxidative phosphorylation (OxPhos) enzymes, and c) severely affects cardiac performance. Hearts from P2rx7-deleted versus WT mice are larger, heart mitochondria smaller, and stroke volume (SV), ejection fraction (EF), fractional shortening (FS) and cardiac output (CO), are significantly decreased. Accordingly, physical fitness of P2X7R-null mice is severely reduced. Thus, the P2X7R is a key modulator of mitochondrial energy metabolism and a determinant of physical fitness.

Protective effects of lipoic acid against acrylamide-induced neurotoxicity: involvement of mitochondrial energy metabolism and autophagy

2017 ◽  
Vol 8 (12) ◽  
pp. 4657-4667 ◽  
Author(s):  
Ge Song ◽  
Zhigang Liu ◽  
Luanfeng Wang ◽  
Renjie Shi ◽  
Chuanqi Chu ◽  
...  
Keyword(s):  
Energy Metabolism ◽  
Lipoic Acid ◽  
Redox Status ◽  
Protective Effects ◽  
Mitochondrial Energy Metabolism

Lipoic acid (LA) suppressed acrylamide (ACR)-induced inflammation, redox status disturbance, autophagy, and apoptosis mediated by mitochondria in the SH-SY5Y cells.

scholarly journals Sulforaphane enriched transcriptome of lung mitochondrial energy metabolism and provided pulmonary injury protection via Nrf2 in mice

2019 ◽  
Vol 364 ◽  
pp. 29-44 ◽  
Author(s):  
Hye-Youn Cho ◽  
Laura Miller-DeGraff ◽  
Terry Blankenship-Paris ◽  
Xuting Wang ◽  
Douglas A. Bell ◽  
...  
Keyword(s):  
Energy Metabolism ◽  
Pulmonary Injury ◽  
Mitochondrial Energy Metabolism ◽  
Injury Protection

Mitochondrial Energy Metabolism in Very Premature Neonates

Neonatology ◽  
2002 ◽  
Vol 81 (4) ◽  
pp. 229-235 ◽  
Author(s):  
László Wenchich ◽  
Jiří Zeman ◽  
Hana Hansíková ◽  
Richard Plavka ◽  
Wolfgang Sperl ◽  
...  
Keyword(s):  
Energy Metabolism ◽  
Mitochondrial Energy Metabolism ◽  
Premature Neonates

scholarly journals Antiproliferative, Antiangiogenic, and Antimetastatic Therapy Response by Mangiferin in a Syngeneic Immunocompetent Colorectal Cancer Mouse Model Involves Changes in Mitochondrial Energy Metabolism

2021 ◽  
Vol 12 ◽  
Author(s):  
Julio César Rodriguez-Gonzalez ◽  
Ivones Hernández-Balmaseda ◽  
Ken Declerck ◽  
Claudina Pérez-Novo ◽  
Emilie Logie ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Fatty Acid ◽  
Energy Metabolism ◽  
Mouse Model ◽  
Mangifera Indica ◽  
High Rate ◽  
Pathway Enrichment Analysis ◽  
Colon Cells ◽  
Mitochondrial Energy Metabolism

In spite of the current advances and achievements in cancer treatments, colorectal cancer (CRC) persists as one of the most prevalent and deadly tumor types in both men and women worldwide. Drug resistance, adverse side effects and high rate of angiogenesis, metastasis and tumor relapse remain one of the greatest challenges in long-term management of CRC and urges need for new leads of anticancer drugs. We demonstrate that CRC treatment with the phytopharmaceutical mangiferin (MGF), a glucosylxanthone present in Mango tree stem bark and leaves (Mangifera Indica L.), induces dose-dependent tumor regression and decreases lung metastasis in a syngeneic immunocompetent allograft mouse model of murine CT26 colon carcinoma, which increases overall survival of mice. Antimetastatic and antiangiogenic MGF effects could be further validated in a wound healing in vitro model in human HT29 cells and in a matrigel plug implant mouse model. Interestingly, transcriptome pathway enrichment analysis demonstrates that MGF inhibits tumor growth, metastasis and angiogenesis by multi-targeting of mitochondrial oxidoreductase and fatty acid β-oxidation metabolism, PPAR, SIRT, NFκB, Stat3, HIF, Wnt and GP6 signaling pathways. MGF effects on fatty acid β-oxidation metabolism and carnitine palmitoyltransferase 1 (CPT1) protein expression could be further confirmed in vitro in human HT29 colon cells. In conclusion, antitumor, antiangiogenic and antimetastatic effects of MGF treatment hold promise to reduce adverse toxicity and to mitigate therapeutic outcome of colorectal cancer treatment by targeting mitochondrial energy metabolism in the tumor microenvironment.

Sign in / Sign up

Export Citation Format

Share Document