The Role of Cellular Stress in Intrauterine Growth Restriction and Postnatal Dysmetabolism

Oke, Shelby L; Hardy, Daniel B.

doi:10.3390/ijms22136986

Cited by 24 publications

(16 citation statements)

References 117 publications

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“…Elevated OS can induce complications in pregnancy progression, leading to long-term effects on both the mother and the fetus. These links were recently reviewed for recurrent pregnancy loss (RPL) [ 1 ], prematurity [ 2 ], intra-uterine growth restriction (IUGR) [ 3 ], diabetes [ 4 ], and preeclampsia, PE [ 5 ].…”

Section: Introductionmentioning

confidence: 99%

The Impact of Oxidative Stress of Environmental Origin on the Onset of Placental Diseases

2022

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Oxidative stress (OS) plays a pivotal role in placental development; however, abnormal loads in oxidative stress molecules may overwhelm the placental defense mechanisms and cause pathological situations. The environment in which the mother evolves triggers an exposure of the placental tissue to chemical, physical, and biological agents of OS, with potential pathological consequences. Here we shortly review the physiological and developmental functions of OS in the placenta, and present a series of environmental pollutants inducing placental oxidative stress, for which some insights regarding the underlying mechanisms have been proposed, leading to a recapitulation of the noxious effects of OS of environmental origin upon the human placenta.

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Section: Introductionmentioning

confidence: 99%

The Impact of Oxidative Stress of Environmental Origin on the Onset of Placental Diseases

2022

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“…Oxidative stress and cellular senescence are also observed in fetal growth restriction [ 31 , 32 , 33 ]. Increased malondialdehyde levels [ 34 ], urinary 8-oxo-7,8 dihydro-deoxyguanosine, and plasma protein carbonylation, but decreased total antioxidant capacity, have been mentioned in the blood sample of pregnant women with growth-restricted fetuses [ 35 ], all of which are also consistent with similar observations in the cord blood of IUGR neonates [ 35 , 36 , 37 ].…”

Section: Introductionmentioning

confidence: 99%

Stress-Induced Premature Senescence Related to Oxidative Stress in the Developmental Programming of Nonalcoholic Fatty Liver Disease in a Rat Model of Intrauterine Growth Restriction

et al. 2022

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Metabolic syndrome (MetS) refers to cardiometabolic risk factors, such as visceral obesity, dyslipidemia, hyperglycemia/insulin resistance, arterial hypertension and non-alcoholic fatty liver disease (NAFLD). Individuals born after intrauterine growth restriction (IUGR) are particularly at risk of developing metabolic/hepatic disorders later in life. Oxidative stress and cellular senescence have been associated with MetS and are observed in infants born following IUGR. However, whether these mechanisms could be particularly associated with the development of NAFLD in these individuals is still unknown. IUGR was induced in rats by a maternal low-protein diet during gestation versus. a control (CTRL) diet. In six-month-old offspring, we observed an increased visceral fat mass, glucose intolerance, and hepatic alterations (increased transaminase levels, triglyceride and neutral lipid deposit) in male rats with induced IUGR compared with the CTRL males; no differences were found in females. In IUGR male livers, we identified some markers of stress-induced premature senescence (SIPS) (lipofuscin deposit, increased protein expression of p21WAF, p16INK4a and Acp53, but decreased pRb/Rb ratio, foxo-1 and sirtuin-1 protein and mRNA expression) associated with oxidative stress (higher superoxide anion levels, DNA damages, decreased Cu/Zn SOD, increased catalase protein expression, increased nfe2 and decreased keap1 mRNA expression). Impaired lipogenesis pathways (decreased pAMPK/AMPK ratio, increased pAKT/AKT ratio, SREBP1 and PPARγ protein expression) were also observed in IUGR male livers. At birth, no differences were observed in liver histology, markers of SIPS and oxidative stress between CTRL and IUGR males. These data demonstrate that the livers of IUGR males at adulthood display SIPS and impaired liver structure and function related to oxidative stress and allow the identification of specific therapeutic strategies to limit or prevent adverse consequences of IUGR, particularly metabolic and hepatic disorders.

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“…With the rapid development of the "Developmental Origins of Health and Disease" theory, associations between fetal-stage adverse events and adulthood diseases have been well established (1,2). The placenta and womb generate an intrauterine environment that protects the fetus from harmful external stimulation, ideally ensuring normal fetal development (3).…”

Section: Introductionmentioning

confidence: 99%

Intrauterine Growth Restriction Induces Adulthood Chronic Metabolic Disorder in Cardiac and Skeletal Muscles

Lan

et al. 2022

Front. Nutr.

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ObjectiveAlthough population-based studies of intrauterine growth restriction (IUGR) demonstrated a series of postnatal complications, several studies identified that IUGR could definitely cause dysfunction of metabolism of cardiac and skeletal muscles in the perinatal period and early life. However, it is still unknown if such metabolic alternation would remain for long term or not, and whether normal protein diet administration postnatally would protect the IUGR offsprings from a “catch-up growth” and be able to reverse the premature metabolic remodeling.Materials and MethodsWe established an IUGR rat model with pregnant rats and a low-protein diet, and the developmental phenotypes had been carefully recorded. The cardiac and skeletal muscles had been collected to undergo RNA-seq.ResultsAccording to a series of comparisons of transcriptomes among various developmental processes, programmed metabolic dysfunction and chronic inflammation activity had been identified by transcriptome sequencing in IUGR offsprings, even such rats presented a normal developmental curve or body weight after normal postnatal diet feeding.ConclusionThe data revealed that IUGR had a significant adverse impact on long-term cardiovascular function in rats, even they exhibit good nutritional status. So that, the fetal stage adverse events would encode the lifelong disease risk, which could hide in young age. This study remaindered that the research on long-term molecular changes is important, and only nutrition improvement would not totally reverse the damage of IUGR.

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The Role of Cellular Stress in Intrauterine Growth Restriction and Postnatal Dysmetabolism

Cited by 24 publications

References 117 publications

The Impact of Oxidative Stress of Environmental Origin on the Onset of Placental Diseases

The Impact of Oxidative Stress of Environmental Origin on the Onset of Placental Diseases

Stress-Induced Premature Senescence Related to Oxidative Stress in the Developmental Programming of Nonalcoholic Fatty Liver Disease in a Rat Model of Intrauterine Growth Restriction

Intrauterine Growth Restriction Induces Adulthood Chronic Metabolic Disorder in Cardiac and Skeletal Muscles

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