Evidence map›Paper›PMID 40933917›Full record

ArticleDrug design, development and therapy2025

Astaxanthin Promotes Spermatogenesis in Mice by Reducing Mitochondrial Oxidative Stress Damage and Regulating Fatty Acid Metabolism and Ferroptosis.

Huang Liu, Xuren Chen, Xin Feng, Zhiyong Zhu, Zhiwei Liao, Shenghui Zhu, Tao Pang, Xuejun Ren, Ruilin Yang

Abstract read
In one paragraph

Article in Drug design, development and therapy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing 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

7 citing papers in PubMed.

  1. Gut Microbiota-Derived Short-Chain Fatty Acids Driven by N-Carbamylglutamate Alleviates Premature Ovarian Failure Through Suppressing Ferroptosis.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.

Huang Liu *Department of Andrology, National Health Commission (NHC) Key Laboratory of Male Reproduction and Genetics, Guangdong Provincial Reproductive Science Institute (Guangdong Provincial Fertility Hospital), Human Sperm Bank of Guangdong Province, Guangzhou, Guangdong, 510600, People's Republic of China.ORCID 0000-0001-8889-9054
Xuren Chen *Department of Andrology, the First Affiliated Hospital of Sun Yat-Sen University, Guangzhou, Guangdong, 510080, People's Republic of China.
Xin Feng *Department of Urology and Andrology, the First Affiliated Hospital of Sun Yat-sen University., Guangzhou, Guangdong, 510080, People's Republic of China.
Zhiyong ZhuDepartment of Andrology, National Health Commission (NHC) Key Laboratory of Male Reproduction and Genetics, Guangdong Provincial Reproductive Science Institute (Guangdong Provincial Fertility Hospital), Human Sperm Bank of Guangdong Province, Guangzhou, Guangdong, 510600, People's Republic of China.
Zhiwei LiaoRadiotherapy Department Area 4, Affiliated Cancer Hospital and Institute of Guangzhou Medical University, Guangzhou, Guangdong, 510095, People's Republic of China.
Shenghui ZhuDepartment of Andrology, National Health Commission (NHC) Key Laboratory of Male Reproduction and Genetics, Guangdong Provincial Reproductive Science Institute (Guangdong Provincial Fertility Hospital), Human Sperm Bank of Guangdong Province, Guangzhou, Guangdong, 510600, People's Republic of China.
Tao PangDepartment of Andrology, National Health Commission (NHC) Key Laboratory of Male Reproduction and Genetics, Guangdong Provincial Reproductive Science Institute (Guangdong Provincial Fertility Hospital), Human Sperm Bank of Guangdong Province, Guangzhou, Guangdong, 510600, People's Republic of China.
Xuejun RenGuangdong Xingding Health Management Co., Ltd., Zhongshan, Guangdong, 528400, People's Republic of China.
Ruilin YangDepartment of Andrology, the Affiliated Panyu Central Hospital of Guangzhou Medical University, Guangzhou, 511400, People's Republic of China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Spermatogenesis is a complex process that affects the outcome of fertility. Different types of cellular metabolic processes have both positive and negative effects on sperm production. Exploring new methods to promote spermatogenesis is the best way to improve fertility. This study confirmed the effect of astaxanthin on promoting spermatogenesis through various experiments. Objective: To explore new activities of astaxanthin and develop the new methods to promote spermatogenesis. Methods: Network pharmacology, in vitro cell culture and in vivo experiments were used in this research. The targets and potential signaling pathways of astaxanthin in the treatment of spermatogenesis, the effects on the proliferation and apoptosis of spermatogonial stem cells, and the therapeutic effect on oligoasthenozoospermia in mice induced with cyclophosphamide of astaxanthin were all observed. The ACSL3, VDAC, GPX4, FADS2, GLS2, Steap3, MDA, GSH-Px, and iron ions were detected and analyzed to reveal the potential regulatory mechanisms. Results: Astaxanthin has 52 key targets for treating spermatogenesis, among which the oxidative stress metabolic pathway is one of the most important factors. The sperm concentration and forward motility of the oligoasthenozoospermia model mice fed with astaxanthin were significantly greater than those of the control group. The proliferation rate of spermatogonial stem cells cultured with astaxanthin was also significantly greater than that of quercetin group and the proportion of apoptotic cells was significantly lower. Astaxanthin can reduce ACSL3, MDA, and iron ions in spermatogonial stem cells; increase the expression of Steap3, VDAC, GPX4, GLS2, GSH-Px, and FADS2; and improve ester metabolism to promote spermatogenesis in oligoasthenozoospermia model mice. Conclusion: Astaxanthin can regulate the metabolism of fatty acid through the ferroptosis pathway, and reduce the mitochondrial oxidative stress damage, and further regulate FADS2, Steap3, and other factors to promote spermatogenesis.

Indexed as

Fatty AcidsFerroptosisMitochondriaOxidative StressSpermatogenesisAnimalsCell ProliferationCells, CulturedMaleMiceXanthophyllsastaxanthineFatty AcidsXanthophyllsastaxanthinfatty acid metabolismferroptosisoxidative stress damagespermatogenesis

Identifiers

PMID40933917
PMCPMC12417715

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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.