Ask about this productRelated genes to: IGFBP7 Blocking Peptide
- Gene:
- IGFBP7 NIH gene
- Name:
- insulin like growth factor binding protein 7
- Previous symbol:
- -
- Synonyms:
- MAC25, IGFBP-7, PSF, FSTL2
- Chromosome:
- 4q12
- Locus Type:
- gene with protein product
- Date approved:
- 1998-03-02
- Date modifiied:
- 2015-11-12
Related products to: IGFBP7 Blocking Peptide
Related articles to: IGFBP7 Blocking Peptide
- Relationships between the concentration of circulating IGFBP-7 and risk of disease and mortality have been suggested by small-scale investigations. In this prospective study, we investigated these relationships among 53,003 UK Biobank participants. Higher IGFBP-7 level was significantly associated with increased risk for liver cancer, all-cause mortality, diabetes, and other diseases. Associations were robust across sex and age groups and persisted over long follow-up. IGFBP-7 polygenic risk scores also predicted cancer and mortality risk. IGFBP-7 level was strongly correlated with levels of previously identified aging-related proteins, but after adjustment for these proteins, remained associated with risk of bladder cancer, liver cancer, multiple myeloma, all-cause mortality, liver-related mortality, and diabetes. Our findings indicate IGFBP-7 as a novel biomarker of mortality and disease risk. - Source: PubMed
Publication date: 2026/05/09
Li ZhiTao ChengzheZhou ZiyiPollak Michael NGiovannucci Edward LSong Mingyang - Immune checkpoint inhibitors (ICIs) are prone to induce cardiovascular adverse reactions during the immunotherapy of cancer patients, among which ICIs-related myocarditis is the most severe. Mitophagy dysregulation is associated with various heart diseases, but its role in ICIs-related myocarditis remains unclear. - Source: PubMed
Publication date: 2026/04/21
Yu JianWang JiangtaoLiu XinyaShi JingZhang YangWang CancanWu LiZhang Yuanming - Pediatric acute kidney injury (AKI) often presents insidiously and progresses rapidly. Traditional diagnostic criteria based on serum creatinine and urine output are markedly delayed and insufficient to capture injury patterns across different etiologies. This paper aims to summarize recent advances in pediatric AKI biomarker research since the release of the ADQI 23 (2020) consensus. Focusing on three major clinical scenarios-cardiac surgery, sepsis, and nephrotoxic drugs-it reviews early biomarker evidence and explores their potential applications in risk stratification. At the mechanistic level, this paper outlines key pathological pathways in pediatric AKI progression: oxygenation-perfusion imbalance after cardiac surgery, endothelium-immune dysregulation driven by sepsis, and tubular-mitochondrial injury associated with nephrotoxic exposure. In CS-AKI, uNGAL shows the earliest elevation within hours after cardiopulmonary bypass, followed by sequential changes in IL-18, L-FABP, and KIM-1. [TIMP-2] × [IGFBP7] and exosomal miRNA aid in identifying high-risk or severe AKI. In SA-AKI, suPAR and glycocalyx/endothelial injury markers (e.g., syndecan-1, Angpt-2/sTM/Tie-2), combined with urinary DKK3 and complement Ba, can be used for early risk stratification and predicting poor outcomes. In NT-AKI, uNGAL has high negative predictive value for excluding severe AKI, while uKIM-1, uCysC, uOPN, and multi-biomarker combinations can indicate subclinical tubular injury earlier after drug exposure. Overall, single biomarkers struggle to cover AKI heterogeneity. Future efforts should integrate functional dynamic assessments (e.g., FST, RRI), scenario-based multi-biomarker combinations, and AI dynamic models to propose evidence-based, scenario-stratified identification pathways. These will serve as structured references for prospective studies and clinical workflow optimization. - Source: PubMed
Publication date: 2026/05/06
Jin WenqinYe QingCheng Dongqing - Acute kidney injury (AKI) is a life-threatening condition whose early diagnosis is crucial. The most used method to evaluate renal function is the glomerular filtration rate (eGFR). The detection of new circulating molecules has gained traction for the early identification of kidney damage. In this prospective observational study, 57 patients with acute kidney disease and 23 patients without acute renal damage were consecutively enrolled; urinary concentrations of NGAL, LFABP, CYR61, TIMP-2, IGFBP-7, and [TIMP-2 X IGFBP-7], and serum concentrations of PENK and KIM-1 were obtained in all patients. The primary endpoint was to assess the role of serum and urinary markers in distinguishing prerenal from renal pathogenesis of AKI. The secondary endpoint was to evaluate the possible association between urinary and serum concentrations of these markers and the severity of acute kidney injury. Urinary TIMP-2, NGAL, and IGFBP-7 concentrations were higher in patients with AKI compared with the control group, with statistical significance. Among patients with AKI, we found higher concentrations of LFABP, Cyr61, TIMP-2, NGAL, IGFBP-7, and [TIMP-2]x[IGFBP-7] according to AKI aetiology, with statistical significance maintained in multivariable logistic regression for IGFBP-7. The ROC curve confirmed that IGFBP-7 has a predictive role in the aetiological diagnosis of AKI. A significant association between urinary LFABP and TIMP-2 and serum KIM-1 concentrations (p = 0.0001) and the variation in creatinine values from baseline to enrollment was found. Furthermore, we found a statistically significant correlation between KIM-1 and the variation in creatinine levels from admission to discharge. This study highlights an association between the concentrations of the novel biomarkers and the aetiology of AKI, with a possible role for these molecules in stratifying patients with acute renal disease. - Source: PubMed
Publication date: 2026/05/04
Pacinella GaetanoBasso Maria GraziaMiceli GiuseppeCasuccio AlessandraDaidone MarioScaglione StefaniaTodaro FedericaPintus ChiaraRizzo GiulianaTuttolomondo Antonino - Heart failure (HF) remains a leading cause of morbidity and mortality worldwide despite major advances in pharmacological and device-based therapies. A central limitation of current treatments is their predominant focus on neurohumoral modulation rather than the intrinsic biological processes driving cardiac remodeling. Recent progress in genetics, single-cell and spatial omics, and systems biology has fundamentally reshaped our understanding of HF, revealing it as a heterogeneous, multicellular syndrome characterized by disrupted intercellular communication within the cardiac cellular ecosystem. Endothelial cells, fibroblasts, immune cells, and cardiomyocytes engage in dynamic signaling networks that coordinate myocardial structure, metabolism, and function; pathological remodeling emerges when these networks become maladaptive. Circulating biomarkers increasingly serve as readouts of these intercellular interactions, reflecting senescence, inflammation, fibrosis, and metabolic stress. Among them, insulin-like growth factor-binding protein 7 has emerged as a key mediator linking endothelial cell senescence to cardiomyocyte metabolic dysfunction. In parallel, stress-activated fibroblast subpopulations drive HF progression through paracrine signaling pathways such as the MYC-CXCL1-CXCR2 axis. These insights open new therapeutic opportunities beyond conventional pharmacology. Immunization-based strategies targeting pathological intercellular communication represent a novel paradigm for disease-modifying HF therapy. Peptide-based vaccines that neutralize circulating mediators or eliminate pathogenic cell populations have demonstrated efficacy in preclinical models and early clinical studies. In this review, we integrate emerging trends in HF research with recent advances in multicellular biology and therapeutic vaccination, proposing immunization as a unifying strategy to target cardiac remodeling at its roots. - Source: PubMed
Publication date: 2026/04/29
Katoh ManamiNomura SeitaroKo ToshiyukiKomuro JinHayashi HirokiNakagami HironoriKomuro Issei