Bioenergetics adaptations and redox homeostasis in pregnancy and related disorders

被引:6
作者
Sanchez-Aranguren, Lissette [1 ]
Nadeem, Sarah [1 ]
机构
[1] Aston Univ, Coll Hlth & Life Sci, Aston Med Sch, Birmingham, W Midlands, England
关键词
Pregnancy; Mitochondria; Mitochondrial dysfunction; Mitochondrial-targeted drugs; INTRAUTERINE GROWTH RESTRICTION; MITOCHONDRIAL-FUNCTION; OXIDATIVE STRESS; PLACENTAL APOPTOSIS; LIPID-METABOLISM; TROPHOBLAST DIFFERENTIATION; ANTIANGIOGENIC FACTORS; ENERGY-METABOLISM; PREECLAMPSIA; RESPIRATION;
D O I
10.1007/s11010-021-04215-0
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Pregnancy is a challenging physiological process that involves maternal adaptations to the increasing energetics demands imposed by the growing conceptus. Failure to adapt to these requirements may result in serious health complications for the mother and the baby. The mitochondria are biosynthetic and energy-producing organelles supporting the augmented energetic demands of pregnancy. Evidence suggests that placental mitochondria display a dynamic phenotype through gestation. At early stages of pregnancy placental mitochondria are mainly responsible for the generation of metabolic intermediates and reactive oxygen species (ROS), while at later stages of gestation, the placental mitochondria exhibit high rates of oxygen consumption. This review describes the metabolic fingerprint of the placental mitochondria at different stages of pregnancy and summarises key signs of mitochondrial dysfunction in pathological pregnancy conditions, including preeclampsia, gestational diabetes and intrauterine growth restriction (IUGR). So far, the effects of placental-driven metabolic changes governing the metabolic adaptations occurring in different maternal tissues in both, healthy and pathological pregnancies, remain to be uncovered. Understanding the function and molecular aspects of the adaptations occurring in placental and maternal tissue's mitochondria will unveil potential targets for further therapeutic exploration that could address pregnancy-related disorders. Targeting mitochondrial metabolism is an emerging approach for regulating mitochondrial bioenergetics. This review will also describe the potential therapeutic use of compounds with a recognised effect on mitochondria, for the management of preeclampsia.
引用
收藏
页码:4003 / 4018
页数:16
相关论文
共 136 条
[11]   What is oxidative stress? [J].
Betteridge, DJ .
METABOLISM-CLINICAL AND EXPERIMENTAL, 2000, 49 (02) :3-8
[12]   Gestational Diabetes Is Characterized by Reduced Mitochondrial Protein Expression and Altered Calcium Signaling Proteins in Skeletal Muscle [J].
Boyle, Kristen E. ;
Hwang, Hyonson ;
Janssen, Rachel C. ;
DeVente, James M. ;
Barbour, Linda A. ;
Hernandez, Teri L. ;
Mandarino, Lawrence J. ;
Lappas, Martha ;
Friedman, Jacob E. .
PLOS ONE, 2014, 9 (09)
[13]   Mitochondrial energy metabolism and ageing [J].
Bratic, Ivana ;
Trifunovic, Aleksandra .
BIOCHIMICA ET BIOPHYSICA ACTA-BIOENERGETICS, 2010, 1797 (6-7) :961-967
[14]   Regulation of the Apaf-1-caspase-9 apoptosome [J].
Bratton, Shawn B. ;
Salvesen, Guy S. .
JOURNAL OF CELL SCIENCE, 2010, 123 (19) :3209-3214
[15]   Maternal overweight and obesity and risk of congenital heart defects in offspring [J].
Brite, J. ;
Laughon, S. k ;
Troendle, J. ;
Mills, J. .
INTERNATIONAL JOURNAL OF OBESITY, 2014, 38 (06) :878-882
[16]   Mitochondrial function as a therapeutic target in heart failure [J].
Brown, David A. ;
Perry, Justin B. ;
Allen, Mitchell E. ;
Sabbah, Hani N. ;
Stauffer, Brian L. ;
Shaikh, Saame Raza ;
Cleland, John G. F. ;
Colucci, Wilson S. ;
Butler, Javed ;
Voors, Adriaan A. ;
Anker, Stefan D. ;
Pitt, Bertram ;
Pieske, Burkert ;
Filippatos, Gerasimos ;
Greene, Stephen J. ;
Gheorghiade, Mihai .
NATURE REVIEWS CARDIOLOGY, 2017, 14 (04) :238-250
[17]   Combining metformin and sulfasalazine additively reduces the secretion of antiangiogenic factors from the placenta: Implications for the treatment of preeclampsia [J].
Brownfoot, Fiona C. ;
Hastie, Roxanne ;
Hannan, Natalie J. ;
Cannon, Ping ;
Nguyen, Tuong, V ;
Tuohey, Laura ;
Cluver, Cathy ;
Tong, Stephen ;
Kaitu'u-Lino, Tu'uhevaha J. .
PLACENTA, 2020, 95 :78-83
[18]   Metformin as a prevention and treatment for preeclampsia: effects on soluble fms-like tyrosine kinase 1 and soluble endoglin secretion and endothelial dysfunction [J].
Brownfoot, Fiona C. ;
Hastie, Roxanne ;
Hannan, Natalie J. ;
Cannon, Ping ;
Tuohey, Laura ;
Parry, Laura J. ;
Senadheera, Sevvandi ;
Illanes, Sebastian E. ;
Kaitu'u-Lino, Tu'uhevaha J. ;
Tong, Stephen .
AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY, 2016, 214 (03) :356.e1-356.e15
[19]  
Butte NF, 2000, AM J CLIN NUTR, V71, p1256S, DOI 10.1093/ajcn/71.5.1256s
[20]   Mitochondria as signaling organelles [J].
Chandel, Navdeep S. .
BMC BIOLOGY, 2014, 12