PMID- 28251550
OWN - NLM
STAT- MEDLINE
DCOM- 20180426
LR  - 20220801
IS  - 1720-8386 (Electronic)
IS  - 0391-4097 (Linking)
VI  - 40
IP  - 8
DP  - 2017 Aug
TI  - The mystery of puberty initiation: genetics and epigenetics of idiopathic central 
      precocious puberty (ICPP).
PG  - 789-802
LID - 10.1007/s40618-017-0627-9 [doi]
AB  - Puberty is a major developmental stage. Damaging mutations, considered as 
      "mistakes of nature", have contributed to the unraveling of the networks 
      implicated in the normal initiation of puberty. Genes involved in the abnormal 
      hypothalamic-pituitary-gonadal (HPG) axis development, in the normosmic 
      idiopathic hypogonadotropic hypogonadism (nIHH), in the X-linked or autosomal 
      forms of Kallmann syndrome and in precocious puberty have been identified (GNRH1, 
      GNRHR, KISS1, GPR54, FGFR1, FGF8, PROK2, PROKR2, TAC3, TACR3, KAL1, PROK2, 
      PROKR2, CHD7, LEP, LEPR, PC1, DAX1, SF-1, HESX-1, LHX3, PROP-1). Most of them 
      were found to play critical roles in HPG axis development and regulation, the 
      embryonic GnRH neuronal migration and secretion, the regulation and action of the 
      hypothalamic GnRH. However, the specific neural and molecular mechanisms 
      triggering GnRH secretion remain one of the scientific enigmas. Although GnRH 
      neurons are probably capable of autonomously generating oscillations, many 
      gonadal steroid-dependent and -independent mechanisms have also been proposed. It 
      is now well proven that the secretion of GnRH is regulated by kisspeptin as well 
      as by permissive or opposing signals mediated by neurokinin B and dynorphin. 
      These three supra-GnRH regulators compose the kisspeptin-neurokinin B-dynorphin 
      neuronal (KNDy) system, a key player in pubertal onset and progression. Moreover, 
      an ongoing increasing number of inhibitory, stimulatory and permissive networks 
      acting upstream on GnRH neurons, such as GABA, NPY, LIN28B, MKRN3 and others 
      integrate diverse hormonal and peripheral signals and have been proposed as the 
      "gate-keepers" of puberty, while epigenetic modifications play also an important 
      role in puberty initiation.
FAU - Leka-Emiri, Sofia
AU  - Leka-Emiri S
AD  - Division of Endocrinology, Diabetes and Metabolism, First Department of 
      Pediatrics, Faculty of Medicine, National and Kapodistrian University of Athens, 
      Medical School, "Aghia Sofia" Children's Hospital, Athens, Greece.
FAU - Chrousos, George P
AU  - Chrousos GP
AD  - Division of Endocrinology, Diabetes and Metabolism, First Department of 
      Pediatrics, Faculty of Medicine, National and Kapodistrian University of Athens, 
      Medical School, "Aghia Sofia" Children's Hospital, Athens, Greece.
FAU - Kanaka-Gantenbein, Christina
AU  - Kanaka-Gantenbein C
AD  - Division of Endocrinology, Diabetes and Metabolism, First Department of 
      Pediatrics, Faculty of Medicine, National and Kapodistrian University of Athens, 
      Medical School, "Aghia Sofia" Children's Hospital, Athens, Greece. 
      c.kanaka-gantenbein@med.uoa.gr.
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20170301
PL  - Italy
TA  - J Endocrinol Invest
JT  - Journal of endocrinological investigation
JID - 7806594
SB  - IM
MH  - *Epigenesis, Genetic
MH  - Humans
MH  - Puberty, Precocious/*genetics/*pathology
OTO - NOTNLM
OT  - Epigenetics
OT  - Genetics
OT  - Idiopathic central precocious puberty
OT  - Puberty onset
EDAT- 2017/03/03 06:00
MHDA- 2018/04/27 06:00
CRDT- 2017/03/03 06:00
PHST- 2017/01/21 00:00 [received]
PHST- 2017/01/25 00:00 [accepted]
PHST- 2017/03/03 06:00 [pubmed]
PHST- 2018/04/27 06:00 [medline]
PHST- 2017/03/03 06:00 [entrez]
AID - 10.1007/s40618-017-0627-9 [pii]
AID - 10.1007/s40618-017-0627-9 [doi]
PST - ppublish
SO  - J Endocrinol Invest. 2017 Aug;40(8):789-802. doi: 10.1007/s40618-017-0627-9. Epub 
      2017 Mar 1.