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This fundamental property is supported by the flagellum, an evolutionarily conserved organelle, which contains dynein motor proteins that provide the mechanical force for sperm propulsion and motility. Primary motility of the sperm cells is acquired during their transit through the epididymis and hyperactivated motility is acquired throughout the journey in the female genital tract by a process called capacitation. These activation processes rely on the micro\u2010environment of the genital tracts. In particular, during capacitation, a panoply of ion transporters located at the surface of the sperm cells mediate complex ion exchanges, which induce an increase in plasma membrane fluidity, the alkalinization of the cytoplasm and protein phosphorylation cascades that are compulsory for sperm hyperactivation and fertilization potential. As a consequence, both structural and functional defects of the sperm flagellum can affect sperm motility, resulting in asthenozoospermia, which constitutes the most predominant pathological condition associated with human male infertility.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Objectives<\/jats:title>\n                    <jats:p>Herein, we have performed a literature review to provide a comprehensive description of the recent advances in the genetics of human asthenozoospermia.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results and Discussion<\/jats:title>\n                    <jats:p>We describe the currently knowledge on gene mutations that affect sperm morphology and motility, namely, asthenoteratozoospermia; we also specify the gene mutations that exclusively affect sperm function and activation, resulting in functional asthenozoospermia. We discuss the benefit of this knowledge for patient and couple management, in terms of genetic counselling and diagnosis of male infertility as a sole phenotype or in association with ciliary defects. Last, we discuss the current strategies that have been initiated for the development of potential therapeutical and contraceptive strategies targeting genes that are essential for sperm function and activation.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/andr.13828","type":"journal-article","created":{"date-parts":[[2025,1,3]],"date-time":"2025-01-03T02:51:57Z","timestamp":1735872717000},"page":"1044-1064","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":25,"title":["Human asthenozoospermia: Update on genetic causes, patient management, and clinical strategies"],"prefix":"10.1111","volume":"13","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-9652-1094","authenticated-orcid":false,"given":"Emma","family":"Cavarocchi","sequence":"first","affiliation":[{"name":"Institute for Advanced Biosciences INSERM U 1209, CNRS UMR 5309, Universit\u00e9 Grenoble Alpes, Team \u201cPhysiopathology and Pathophysiology of Sperm Cells\u201d  Grenoble France"},{"name":"Faculty of Medicine Centre Hospitalier Universitaire de Qu\u00e9bec\u2010Research Center, Department of Obstetrics, Gynecology, and Reproduction, Universit\u00e9 Laval  Quebec Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ma\u00ebva","family":"Drouault","sequence":"additional","affiliation":[{"name":"Institute for Advanced Biosciences INSERM U 1209, CNRS UMR 5309, Universit\u00e9 Grenoble Alpes, Team \u201cPhysiopathology and Pathophysiology of Sperm Cells\u201d  Grenoble France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Joao C.","family":"Ribeiro","sequence":"additional","affiliation":[{"name":"Institute for Advanced Biosciences INSERM U 1209, CNRS UMR 5309, Universit\u00e9 Grenoble Alpes, Team \u201cPhysiopathology and Pathophysiology of Sperm Cells\u201d  Grenoble France"},{"name":"Unit for Multidisciplinary Research in Biomedicine, Institute of Biomedical Sciences Abel Salazar University of 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