Evidence map›Paper›PMID 40805036›Full record

ReviewAnimals : an open access journal from MDPI2025

Mitochondrial Regulation of Spermatozoa Function: Metabolism, Oxidative Stress and Therapeutic Insights.

Zhiqian Xu, Qi Yan, Ke Zhang, Ying Lei, Chen Zhou, Tuanhui Ren, Ning Gao, Fengyun Wen, Xiaoxia Li

Abstract readReview
In one paragraph

Review in Animals : an open access journal from MDPI, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

21 citing papers in PubMed.

  1. Article
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  6. TFEB Deficiency Impairs Male Fertility Through Mitochondrial Dysfunction.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors.

Zhiqian XuCollege of Animal Science and Technology, Henan University of Science and Technology, Luoyang 471023, China.
Qi YanCollege of Animal Science and Technology, Henan University of Science and Technology, Luoyang 471023, China.
Ke ZhangCollege of Animal Science and Technology, Henan University of Science and Technology, Luoyang 471023, China.
Ying LeiCollege of Animal Science and Technology, Henan University of Science and Technology, Luoyang 471023, China.
Chen ZhouCollege of Animal Science and Technology, Henan University of Science and Technology, Luoyang 471023, China.
Tuanhui RenCollege of Animal Science and Technology, Henan University of Science and Technology, Luoyang 471023, China.
Ning GaoCollege of Animal Science and Technology, Hunan Agricultural University, Changsha 410125, China.
Fengyun WenCollege of Animal Science and Technology, Henan University of Science and Technology, Luoyang 471023, China.
Xiaoxia LiCollege of Animal Science and Technology, Henan University of Science and Technology, Luoyang 471023, China.

Funding

Doctoral Scientific Research Foundation of Henan University of Science and Technology 13480096grants from the National Natural Science Foundation of China 32302742Science & Technology Key Project of Henan Provincial Education Department in China 24A230002
6 · The paper itself

Abstract

Mitochondria are central to energy production and redox regulation in spermatozoa, supporting key functions such as progressive motility, capacitation, and the acrosome reaction. These processes are essential for successful fertilization and embryo development. However, species-specific differences exist in the reliance on oxidative phosphorylation versus glycolysis. Mitochondria also generate reactive oxygen species, which at physiological levels aid in sperm function but can cause oxidative stress and damage when overproduced. Mitochondrial dysfunction and excessive ROS can impair membrane potential, induce apoptosis, and damage nuclear and mitochondrial DNA, ultimately compromising sperm quality. Sperm mitochondrial DNA is highly susceptible to mutations and deletions, contributing to reduced motility and fertility. Targeted antioxidant strategies have emerged as promising therapeutic interventions to mitigate oxidative damage. This article provides a comprehensive overview of mitochondrial regulation in spermatozoa, the consequences of redox imbalance, and the potential of mitochondria-targeted antioxidants to improve sperm function and male fertility outcomes. The paper aims to deepen our understanding of mitochondrial roles in sperm physiology and contribute to the advancement of strategies for addressing male infertility.

Indexed as

antioxidantenergy metabolismmitochondriamtDNAreactive oxygen speciesspermatozoa

Identifiers

PMID40805036
PMCPMC12345440

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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 OpenQuestion graph.