Ask about this productRelated genes to: GHRHR Blocking Peptide
- Gene:
- GHRHR NIH gene
- Name:
- growth hormone releasing hormone receptor
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 7p14.3
- Locus Type:
- gene with protein product
- Date approved:
- 1993-06-22
- Date modifiied:
- 2016-10-05
Related products to: GHRHR Blocking Peptide
Related articles to: GHRHR Blocking Peptide
- Heart failure (HF) with preserved ejection fraction (HFpEF) carries a high mortality and remains a major therapeutic challenge. Effective, targeted therapies capable of reversing HFpEF pathophysiology are urgently needed. We previously demonstrated that activation of the cardiac growth hormone-releasing hormone (GHRH) pathway using high potency synthetic agonists of GHRH (GHRH-agonists) improves the HFpEF phenotype in both large and small animal models, including in a murine model of cardiometabolic HFpEF (High fat diet + L-NAME). Here we sought to define the downstream signaling pathways responsible for this effect. A transcriptomic screen in human iPSC-derived cardiomyocytes (hiPSC-CMs) identified the HIF-1α pathway as being activated by GHRH receptor (GHRHR) signaling, revealing an oxygen-independent mechanism of HIF-1α activation. Based on this finding, we investigated the interaction between the cardioprotective effects of the GHRH-agonist MR-356 and HIF-1α pathway activation in the murine HFD+L-NAME model of cardiometabolic HFpEF. We generated a cardiomyocyte-specific HIF-1α knockout (HIF-1αKO) mouse line and demonstrated that our previously reported beneficial effects of GHRH-agonist administration were completely abolished in HIF-1αKO mice. Together, these findings establish the GHRHR-HIF-1α axis as a putative integrative pathway coupling metabolic and contractile remodeling, suggesting that therapeutic targeting of this axis represents a novel disease-modifying approach to treating cardiometabolic HFpEF. - Source: PubMed
Publication date: 2026/08/01
Kanashiro-Takeuchi Rosemeire MTakeuchi Lauro MBalkan WayneAsensi KarinaDulce Raul AWanschel Amarylis C B AHatzistergos Konstantinos EKulandavelu ShathiyahSaltzman Russell GShehadeh Lina ASha WeiSchally Andrew VKurtenbach StefanHare Joshua M - This study evaluated the effects of dietary sulphur-containing amino acid (SAA) levels provided during the early (1-28 d) and late (29-63 d) growth stages on production traits and feather follicle gene expression in 63-day-old Jiangnan white goslings. A total of 288 one-day-old male goslings were assigned to a 2 × 2 factorial design with two early SAA levels (0.64% and 0.87%) and two late SAA levels (0.62% and 0.74%), which created four treatments: Dd (low-low), Dg (low-high), Gd (high-low), and Gg (high-high). All measurements were performed on 63-day-old birds. Final body weight was significantly affected only by early SAA levels ( = 0.03), with the high early groups (Gd and Gg) showing a 3% higher weight (3.99 vs. 3.88 kg) than the low early groups. Late SAA levels had no effect on growth but markedly reduced breast muscle cooking loss ( < 0.01) from 26.64% (low late) to 22.70% (high late), which represents a 15% relative improvement in water-holding capacity. A significant early × late interaction ( = 0.03) indicated that late high SAA levels partially compensated for early deficiency. High late SAA levels also slightly reduced dry matter digestibility (73.45% → 73.16%, = 0.03), while high early SAA levels increased crude ash digestibility (33.59% → 35.66%, = 0.04). The Dg treatment (low early + high late) caused significantly elevated serum low-density lipoprotein (2.06 vs. 1.42-1.58 mmol/L) and uric acid (348.15 vs. 243.60-294.97 μmol/L), which indicates metabolic stress ( < 0.01 and = 0.02 for interaction). Transcriptomic analysis of feather follicles from the Gg and Gd groups (both receiving identical high early SAA supplementation) identified 121 differentially expressed genes, including the downregulation of (cysteine/methionine metabolism) and upregulation of (neuroactive ligand-receptor interaction) in Gg, providing a molecular basis for improved feather growth. q-PCR validated five selected genes. In conclusion, final body weight is determined by early SAA supply, while late SAA supplementation improves meat juiciness, but abrupt increases from low to high SAA levels cause metabolic disturbances. Under this test conditions, The optimal feeding strategy is 0.87% SAAs (1-28 d) followed by 0.74% SAAs (29-63 d). - Source: PubMed
Publication date: 2026/06/17
Liu QingxueNazir UsmanLi XuanXing XiyuanZheng XuchengYang ZhiYang HaimingWang Zhiyue - Growth hormone-releasing hormone (GHRH) antagonists have displayed anti-neoplastic activity against a multitude of cancers in vitro, as well as in vivo, via xenografted tumors in nude mice. Following a successful demonstration of GHRH antagonists treating non-Hodgkin's lymphoma and the discovery of mRNA and peptide products in immune cells, GHRH antagonism was explored in acute myeloid leukemia (AML), a disease characterized by a malignant expansion of immature myeloid progenitors, and poor 5-year survival. Targeted therapies have yielded breakthroughs in treatment response and overall survival, such as all-trans retinoic acid/arsenic trioxide (ATRA/ATO) for acute promyelocytic leukemia (APL), or FLT3 inhibitors, IDH inhibitors, and menin inhibitors for AML harboring actionable genetic lesions. However, therapeutic resistance remains a major barrier to durable remission. GHRH receptor (GHRH-R) has been reported in several experimental models of AML, including drug-resistant sublines. Significant time- and dose-dependent reduction in leukemic growth was observed in vitro and in vivo following MIA-602 treatment. FLT3 inhibitor resistance has been associated with activation of PI3K/AKT, ERK/MAPK, inflammatory, stromal, and apoptotic escape pathways. The documented effects of GHRH-R antagonism raise the possibility that it could influence signaling networks relevant to therapeutic resistance in AML. This hypothesis remains speculative; to date no studies have stratified AML by status in the context of GHRH-R expression or GHRH antagonism, and there is currently no evidence that MIA-602 directly alters FLT3 receptor signaling or inhibitor sensitivity. - Source: PubMed
Publication date: 2026/06/20
Costoya JoelJimenez Joaquin J - Growth hormone deficiency (GHD) is a rare endocrine disorder responsible for growth failure. In the absence of an identified secondary cause, a genetic etiology can be identified, affecting genes involved in hypothalamo-pituitary growth hormone (GH) regulation or in pituitary development itself. The anterior pituitary gland arises from the oral ectoderm and is regulated by neuroectodermal signaling and transcription factors that ensure proper differentiation of hormone-producing cells. GH secretion is stimulated by growth hormone-releasing hormone (GHRH) and ghrelin, with mutations in their respective receptors (GHRHR, GHSR) contributing to isolated GHD (IGHD). Mutations in GH1, encoding GH itself, are the main genetic cause of IGHD. GHD can also arise from mutations in transcription factor genes such as POU1F1, PROP1, IGSF1 or TBX19 or in genes involved in early brain development such as GLI2, LHX3 or HESX1, potentially leading to syndromic presentations with multi-organ involvement. Understanding the genetic basis of GHD is essential to improving diagnostic strategies, genetic counseling and the development of targeted therapies. Although animal models have been fundamental for understanding pituitary ontogenesis, emerging tools such as human pituitary organoids now offer the promise of dissecting human-specific regulatory mechanisms that cannot be fully captured in traditional animal models. This review aims to provide a comprehensive overview of all known genetic causes of GHD, with a particular focus on the underlying molecular mechanisms and their associated phenotypes. - Source: PubMed
Publication date: 2026/06/06
Aouchiche KarineReynaud RachelCharnay TheoCastinetti FrédéricBrue ThierrySaveanu AlexandruBarlier Anne - Pregnancy leads to many adaptations in the maternal body, most of which are reversible. However, reproductive experience can also result in permanent effects. Here, we investigated how pregnancy influences the somatotrophic system and the lasting effects of reproductive experience on the maternal organism. Reproductive experience induced a pronounced increase in lean body mass and longitudinal growth in both wild-type and growth hormone (GH)-deficient mice compared with age-matched virgins. Body growth was primarily observed during the first pregnancy, whereas a second gestation was mostly associated with increased adiposity. Data from a cohort of women with isolated GH deficiency (IGHD) caused by a loss-of-function mutation in the GHRHR gene revealed that nulliparous women were 7 cm shorter than those with one or more pregnancies. Increased GH secretion was observed in pregnant wild-type mice but not in pregnant GHRHR-deficient mice. Pregnancy-induced body growth is preserved despite disruption of GH-, ghrelin-, and estrogen-related signaling pathways. In conclusion, reproductive experience induces permanent changes in the maternal organism, promoting body growth in models that allow this response. Pregnancy-induced body growth appears to be independent of GH action. These findings underscore the need for further studies to investigate the long-lasting consequences of reproductive experience in females. - Source: PubMed
Publication date: 2026/05/05
de Souza Gabriel ODos Santos Willian OWasinski Frederickde Sousa Ligia M MAmaral Andressa GGusmao Daniela OList Edward OKopchick John JFernandez GimenaPerelló MarioOliveira Carla R PAguiar-Oliveira Manuel HDonato Jose