Ask about this productRelated genes to: CRISPLD2 antibody
- Gene:
- CRISPLD2 NIH gene
- Name:
- cysteine rich secretory protein LCCL domain containing 2
- Previous symbol:
- LCRISP2
- Synonyms:
- DKFZP434B044, LGL1
- Chromosome:
- 16q24.1
- Locus Type:
- gene with protein product
- Date approved:
- 2005-02-11
- Date modifiied:
- 2016-11-01
Related products to: CRISPLD2 antibody
Related articles to: CRISPLD2 antibody
- Hepatic fibrosis (HF) is a key pathological process in the development of chronic liver disease, and the activation of hepatic stellate cells (HSCs) is its core driving factor. Although curcumin, as a natural polyphenolic compound, has therapeutic potential, its specific mechanism in HF is still unclear. - Source: PubMed
Liu LingZheng JintaoWang YeYang ChenaoShan YuqiangJia Changku - Liver fibrosis caused by chronic inflammation remains the major driver of various liver diseases. However, limited effective therapies have been identified for liver fibrosis. Herein, we elucidated the complicated molecular mechanisms underlying liver fibrosis. - Source: PubMed
Publication date: 2026/04/24
Zhang HaoyeWang JuanYang HuiYan YuZou JiafengLiu Zhenguo - Bronchopulmonary dysplasia (BPD) is a chronic lung condition in preterm infants characterized by impaired alveolar development, disrupted vascular growth, and persistent inflammation. These alterations, which often arise from early exposure to mechanical ventilation, oxygen toxicity, and infection, can lead to long-term structural and functional deficits in the developing lung. In adulthood, chronic obstructive pulmonary disease (COPD) represents a major cause of morbidity and mortality and is defined by progressive airflow obstruction, reduced respiratory capacity, and chronic inflammatory responses. Although traditionally considered a disease of adult smokers, growing evidence suggests that early-life respiratory insults play a key role in shaping long-term lung health. Recent studies reveal a biologically plausible link between BPD and later COPD, indicating that premature birth, impaired lung growth, and early inflammatory injury may predispose individuals to earlier or more severe COPD development. This review explores the shared molecular pathways connecting these conditions, focusing on overlapping inflammatory biomarkers such as , , , , , and , which collectively reflect persistent dysregulation of immune and repair mechanisms. Additionally, common genetic variants, including and , may contribute to susceptibility across the lifespan. Emerging biomarkers-such as , /, , and -offer further insight into disease progression. Identifying these shared markers may ultimately improve early detection and help clinicians pinpoint infants with BPD who face an elevated risk of developing COPD later in life. - Source: PubMed
Publication date: 2026/01/30
Gambadauro AntonellaXerra FedericaChirico ValeriaRulli ImmacolataCacciola AnnalisaMallamace RaffaellaGitto EloisaMarseglia Lucia Marina - Intervertebral disc degeneration (IVDD) is a major cause of chronic low back pain, yet its molecular mechanisms remain unclear. We identified CRISPLD2 (cysteine-rich secretory protein LCCL domain-containing 2) as a critical regulator of nucleus pulposus cells (NPCs) homeostasis during IVDD. Single-cell transcriptomic analysis (scRNA-seq) revealed degenerative NPCs subsets enriched in iron metabolism and lipid peroxidation. CRISPLD2 knockdown in NPCs led to disrupted redox balance, elevated lipid peroxides, and excessive iron accumulation, promoting oxidative stress-induced ferroptosis and disc degeneration. Mechanistically, we identified a CRISPLD2-miR-548I-IL17A axis that governs ferroptotic cell death in IVDD, where CRISPLD2 deficiency was associated with reduced miR-548I expression, accompanied by subsequent upregulation of IL17A, thereby amplifying inflammatory and oxidative stress responses. In vivo, CRISPLD2 knockdown induced spontaneous IVDD and increased pain sensitivity, while restoration of CRISPLD2 or inhibition of IL17A alleviated ferroptosis and improved NPCs survival. Adeno-associated virus (AAV)-mediated overexpression of CRISPLD2 successfully alleviated IVDD in lumbar spine instability and needle-puncture models, reducing oxidative stress-induced ferroptosis and restoring disc integrity. These findings highlight the critical role of CRISPLD2 in regulating oxidative stress-induced ferroptosis in IVDD and suggest that targeting the CRISPLD2-miR-548I-IL17A axis may provide a novel therapeutic strategy for preventing disc degeneration and alleviating discogenic pain. - Source: PubMed
Publication date: 2026/01/09
Shi YangyangLi FudongZhao TianyiSun KaiqiangZhang DanyingYan ChenXu XimingSun JingchuangHu XulinYong XinShi JiangangWang Yuan - Gestational diabetes mellitus (GDM), one of the prevalent pregnancy-related metabolic disorders, have shown immediate or long-term adverse health outcomes for maternal and fetal health. Therefore, it is crucial to understand the ongoing cellular and molecular changes in GDM patients for characterizing novel biomarkers for diagnosis and therapeutic purposes. In the current study, we analyzed 3 transcriptomic datasets, characterized 449 unique upregulated and 785 downregulated DEGs, and performed several analyses. Gene ontology shows enrichment of migration, development, and immune-related processes in GDM patients. KEGG pathway shows enrichment of pathways like "type 1 diabetes mellitus" and "graft versus host disease". Disease ontology shows enrichment of "female reproductive system disease," "anemia," etc. Integration of methylation and transcriptomic data identified 11 genes (RASSF2, WSCD1, TNFAIP3, TPST1, UBASH3B, ZFP36, CRISPLD2, IGFBP7, TNS3, TPM2, and VTRNA1-2), as potential novel diagnostic biomarkers and therapeutic targets. Furthermore, immune cell-type infiltration analysis shows higher memory B-cells and lower M1 macrophages and CD8 T-cells. Protein-protein interaction analysis followed by ROC analysis in an independent dataset identified 7 hub genes (POLR2G, VWF, COL5A1, COL6A1, CD44, COL3A1, and COL1A1) with high diagnostic potential. Overall, we obtained 18 genes that could serve as novel diagnostic biomarkers and therapeutic targets in GDM patients. - Source: PubMed
Publication date: 2025/09/25
Mitra TridipYadav Dinesh VenkatesanKumari R SajeethaAgrawal PiyushJanardhanan Rajiv