The recently published World Health Organization (WHO) infertility guideline introduces a global approach to infertility care with significant implications for male reproductive health. This review examines the male infertility components of the WHO guideline and compares them with those from the American Urological Association/American Society for Reproductive Medicine (AUA/ASRM), European Association of Urology (EAU), European Society of Human Reproduction and Embryology (ESHRE) and National Institute for Health and Care Excellence (NICE). The WHO guideline adopts a public health perspective, emphasizing infertility prevention, standardized diagnostic algorithms, and the central role of semen analysis, while prioritizing feasibility across diverse healthcare settings. In contrast, AUA/ASRM and EAU guidelines offer comprehensive, specialist-oriented recommendations, including endocrine evaluation, genetic testing, and a wide range of therapeutic interventions, whereas ESHRE and NICE follow a couple-centered approach with limited focus on male-specific pathways. The WHO guideline provides a more selective approach to management, with a neutral stance on antioxidant therapy and specific recommendations for varicocele, highlighting it as a key, potentially treatable condition. Across guidelines, there is broad consensus on core diagnostic principles, but differences remain in scope, depth, and implementation strategies. These variations reflect not only differences in target populations and healthcare contexts but also notable gaps in the evidence base. Strengthening evidence for commonly used interventions, including antioxidants, hormonal therapies, and advanced diagnostics, and promoting greater harmonization across guidelines are essential to advancing male infertility care.

Microplastics and nanoplastics are ubiquitous across global environments and can bioaccumulate through food chains, arousing concerns over their links to rising rates of male infertility. Relevant literature was retrieved from PubMed, Web of Science Core Collection and Scopus, and eligible original human, animal and cell studies were screened and analyzed. Epidemiological data confirm microplastic accumulation in human reproductive tissues, which correlates with declining semen quality. Experimental evidence reveals that microplastics penetrate the blood-testis barrier to trigger testicular oxidative stress, DNA damage and epigenetic dysregulation, further causing inflammation, barrier disruption, hormone imbalance and sustained spermatogenic injury. This review systematically interprets core toxic cascades of microplastic-induced male infertility, and compares heterogeneous reproductive toxicity from varying particle sizes, polymers, doses and combined pollutants. Research gaps and future directions are also outlined, providing theoretical support for assessing male reproductive hazards of microplastic pollution.

The decline in male sperm quality has become a global concern for male reproductive health. Research indicates that heat stress is an important external factor that contributes to male infertility, potentially promoting germ cell apoptosis, disrupting redox balance, and affecting proteostasis. Recently, a growing body of research has demonstrated an association between heat stress-related proteins and male infertility. Heat shock proteins (HSPs) and their upstream transcription factors, known as heat shock factors (HSFs), constitute the core molecular system through which cells respond to heat stress. The main heat-shock protein families, including HSPA1, HSPA2, HSP90, HSP60, and small HSPs Small Heat Shock Proteins, play pivotal regulatory roles in spermatogenesis. These protein families influences the balance between germ cell repair and cell death by regulating proteostasis, oxidative homeostasis, and cell survival. The dysregulation of this system may represent an important molecular basis for heat stress-induced male infertility. This review focuses on the pathophysiological process of heat stress-induced male infertility, summarizes the potential mechanisms by which heat stress and heat stress-related proteins contribute to male infertility, and proposes a dynamic model of HSP systemic responses under heat stress. The current progress in the diagnosis and treatment of heat stress-related male infertility is summarized to provide a theoretical basis for further elucidating its pathogenesis, improving diagnostic accuracy, and guiding the developing of targeted therapeutic strategies.