Journal
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
Volume 18, Issue 2, Pages -Publisher
MDPI
DOI: 10.3390/ijms18020381
Keywords
chronic kidney disease; congenital anomalies of the kidney and urinary tract (CAKUT); developmental origins of health and disease (DOHaD); Epigenetic regulation; nephron endowment; oxidative stress; renin-angiotensin system; sex differences; sodium transporter; transcriptome
Funding
- Ministry of Science and Technology, Taiwan [MOST 104-2314-B-182-056-MY3]
- Chang Gung Memorial Hospital, Kaohsiung, Taiwan [CMRPG8F0251, CMRPG8F0021, CMRPG8F0161]
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Chronic kidney disease (CKD) is becoming a global burden, despite recent advances in management. CKD can begin in early life by so-called developmental programming or developmental origins of health and disease (DOHaD). Early-life insults cause structural and functional changes in the developing kidney, which is called renal programming. Epidemiological and experimental evidence supports the proposition that early-life adverse events lead to renal programming and make subjects vulnerable to developing CKD and its comorbidities in later life. In addition to low nephron endowment, several mechanisms have been proposed for renal programming. The DOHaD concept opens a new window to offset the programming process in early life to prevent the development of adult kidney disease, namely reprogramming. Here, we review the key themes on the developmental origins of CKD. We have particularly focused on the following areas: evidence from human studies support fetal programming of kidney disease; insight from animal models of renal programming; hypothetical mechanisms of renal programming; alterations of renal transcriptome in response to early-life insults; and the application of reprogramming interventions to prevent the programming of kidney disease.
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