Dear Editor,Solute carrier family 26 member 8(SLC26A8)gene belongs to the solute carrier 26(SLC26)family.It demonstrates distinct expression in male spermatozoa.This gene potentially plays a role in the formation of t...Dear Editor,Solute carrier family 26 member 8(SLC26A8)gene belongs to the solute carrier 26(SLC26)family.It demonstrates distinct expression in male spermatozoa.This gene potentially plays a role in the formation of the sperm annulus,a circular structure linking the midpiece and principal piece of mature sperm flagella.1 Studies in mice have shown that the deficiency of Slc26A8 leads to compromised sperm motility,capacitation,and structural anomalies.These include disarray in the mitochondrial sheath,abnormalities in the annulus,and bending of the flagella.2,3 Nevertheless,our comprehension of SLC26A8 mutations in male infertility is still restricted,with only a limited number of studies addressing this aspect.4-6 Therefore,further research is crucial to elucidate the functional significance of mutations in SLC26A8.展开更多
基金support from grants provided by the Gansu Provincial Natural Science Foundation of China(23JRRA1046)the Gansu Association for Science and Technology(GSHZTS 2022-04)the National College Student Innovation and Entrepreneurship Training Program(202310730222).
文摘Dear Editor,Solute carrier family 26 member 8(SLC26A8)gene belongs to the solute carrier 26(SLC26)family.It demonstrates distinct expression in male spermatozoa.This gene potentially plays a role in the formation of the sperm annulus,a circular structure linking the midpiece and principal piece of mature sperm flagella.1 Studies in mice have shown that the deficiency of Slc26A8 leads to compromised sperm motility,capacitation,and structural anomalies.These include disarray in the mitochondrial sheath,abnormalities in the annulus,and bending of the flagella.2,3 Nevertheless,our comprehension of SLC26A8 mutations in male infertility is still restricted,with only a limited number of studies addressing this aspect.4-6 Therefore,further research is crucial to elucidate the functional significance of mutations in SLC26A8.
