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Xiao-Dong Li

Publications and source records attributed to Xiao-Dong Li.

3 recordsLinked to original sources
PubMed2026

Proteomic insights into azoospermia: protein differences in testicular tissue between non-obstructive and obstructive azoospermia patients.

Non-obstructive azoospermia (NOA) and obstructive azoospermia (OA) are the main classifications of severe male infertility, but the molecular mechanism of NOA remains poorly understood. This study aimed to identify potential biomarkers and pathological mechanisms by comparing the proteomic differences in testicular tissues of NOA and OA patients. Through proteomic analysis based on liquid chromatography-tandem mass spectrometry (LC-MS/MS) of testicular samples from 5 NOA patients and 5 OA patients, we identified 5264 proteins, among which 717 differentially expressed proteins (DEPs) were found between the two groups (242 upregulated and 475 downregulated in NOA). Bioinformatics analysis indicated that these DEPs were significantly associated with reproductive development, gametogenesis, and cell structural stability. On the basis of this, six candidate proteins, including dysferlin (DYSF), myoferlin (MYOF), mitsugumin 53 (MG53), cluster of differentiation 63 (CD63), caveolin-3 (CAV3), and calpain-3 (CAPN3), were selected from the DEPs and verified in an expanded sample set (37 NOA cases and 28 OA cases) through quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot, confirming their dysregulation in NOA. These findings provide new proteomic insights into NOA, highlighting the disruption of membrane repair and structural pathways, and offer potential biomarkers for understanding its pathogenesis.

Humans↗
PubMed2025

Targeting IL-16 to Protect Angiotensin II-induced Hypertension and Renal Injury.

BACKGROUND: T cells are critical in the pathogenesis of hypertension. IL (interleukin)-16 is primarily produced and secreted by T cells; however, its role in hypertension remains unclear. METHODS: Serum samples from patients with hypertension were collected and analyzed using ELISA. A mouse model of Ang II (angiotensin II)-induced hypertension was established, and the role of IL-16 was investigated. RESULTS: IL-16 expression was elevated in patients with hypertension and positively correlated with both systolic and diastolic blood pressure. In Ang II-induced hypertensive mice, IL-16 expression was significantly upregulated in serum, kidney, and aortic tissues. IL-16-neutralizing antibody reduced both systolic and diastolic blood pressure in response to Ang II. Histological analyses revealed that renal injury and vascular remodeling were attenuated after IL-16 neutralization. Mechanistically, T-cell-derived IL-16 enhanced CD4+ (cluster of differentiation 4) T helper 1 cell function and mediated crosstalk with macrophages to stimulate inflammatory responses via activation of NF-κB (nuclear factor kappa B) and MAPK (mitogen-activated protein kinase) pathways. Conditioned medium from macrophages primed with IL-16-treated T helper 1 cells promoted smooth muscle cell proliferation and exacerbated endothelial cell damage during hypertension progression. CONCLUSIONS: Collectively, these findings indicate that T-cell-derived IL-16 exacerbates Ang II-induced hypertension and associated organ damage by promoting a T helper 1-macrophage-driven proinflammatory response.

Hypertension↗