Hua-Long Zhu

Area of research

Health, Toxicology and Mutagenesis · Pediatrics, Perinatology and Child Health

Research interest

Research topics from publications: Combination of high-fat diet and cadmium impairs testicular spermatogenesis in an m6A-YTHDF2-dependent manner; Sperm Rhoa m6A modification mediates intergenerational transmission of paternally acquired hippocampal neuronal senescence and cognitive deficits after combined exposure to environmental cadmium and high-fat diet in mice; Environmental cadmium exposure during gestation impairs fetal brain and cognitive function of adult offspring via reducing placenta-derived E2 level; Multigenerational paternal obesity enhances the susceptibility to male subfertility in offspring via Wt1 N6-methyladenosine modification; Advances in immunology of male reproductive toxicity induced by common environmental pollutants; Loss of Atg5 in Sertoli cells enhances the susceptibility of cadmium-impaired testicular spermatogenesis in mice; NBR1-dependent autophagy activation protects against environmental cadmium-evoked placental trophoblast senescence. Representative work: There is strong evidence that obesity is a risk factor for poor semen quality. However, the effects of multigenerational paternal obesity on the susceptibility to cadmium (a reproductive toxicant)-induced spermatogenesis disorders in offspring remain unknown. Here, we show that, in mice, spermatogenesis and retinoic acid levels become progressively lower as the number of generations exposed to a high-fat diet increase. Furthermore, exposing several generations of mice to a high fat diet results in a decrease in the expression of Wt1, a transcription factor upstream of the enzymes that synthesize retinoic acid. These effects can be rescued by injecting adeno-associated virus 9-Wt1 into the mo Humans are exposed to an ever-increasing number of environmental toxicants, some of which have gradually been identified as major risk factors for male reproductive health, even associated with male infertility. Male infertility is usually due to the reproductive system damage, which may be influenced by the exposure to contaminants such as heavy metals, plasticizers, along with genetics and lifestyle. Testicular immune microenvironment (TIM) is important in maintaining normal physiological functions of the testis, whether disturbed TIM after exposure to environmental toxicants could induce reproductive toxicity remains to be explored. Therefore, the current review aims to contribute to

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