ArticleCell and tissue research2023
Quantitative proteomics of sperm tail in asthenozoospermic patients: exploring the molecular pathways affecting sperm motility.
Article in Cell and tissue research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
7 citing papers in PubMed, 6 citations in OpenAlex.
- DCDC2C Protein Expression in Human Spermatozoa: A Potential Molecular Marker for Asthenozoospermia.Medical sciences (Basel, Switzerland) · 2026Article
- High-Resolution Imaging Reveals Mitochondrial Protein Imbalance in Sperm of Oligoasthenospermic Men.Molecular reproduction and development · 2026Article
- A modular, mechanism-informed biomarker panel for asthenozoospermia based on integrative sperm proteomics.Frontiers in endocrinology · 2026Article
- D-Mannose-Mediated metabolic pathways sustain the molecular signatures of sperm function and fertilization.Journal of advanced research · 2025Article
- Deciphering the role of reactive oxygen species in idiopathic asthenozoospermia.Frontiers in endocrinology · 2025Review
- Quantitative Proteomics Reveal Region-Specific Alterations in Neuroserpin-Deficient Mouse Brain and Retina: Insights into Serpini1 Function.Proteomes · 2024Article
- Mitochondrial dysfunction signatures in idiopathic primary male infertility: a validated proteomics-based diagnostic approach.Frontiers in reproductive health · 2024Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 5 countries.
Funding
Abstract
Asthenozoospermia, characterized by low sperm motility, is one of the most common causes of male infertility. While many intrinsic and extrinsic factors are involved in the etiology of asthenozoospermia, the molecular basis of this condition remains unclear. Since sperm motility results from a complex flagellar structure, an in-depth proteomic analysis of the sperm tail can uncover mechanisms underlying asthenozoospermia. This study quantified the proteomic profile of 40 asthenozoospermic sperm tails and 40 controls using TMT-LC-MS/MS. Overall, 2140 proteins were identified and quantified where 156 proteins have not been described earlier in sperm tail. There were 409 differentially expressed proteins (250 upregulated and 159 downregulated) in asthenozoospermia which by far is the highest number reported earlier. Further, bioinformatics analysis revealed several biological processes, including mitochondrial-related energy production, oxidative phosphorylation (OXPHOS), citric acid cycle (CAC), cytoskeleton, stress response, and protein metabolism altered in asthenozoospermic sperm tail samples. Collectively, our findings reveal the importance of mitochondrial energy production and induced stress response as potential mechanisms involved in the loss of sperm motility in asthenozoospermia.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.