The impact of heat on kidney health: A PRISMA-compliant bibliometric analysis.

BACKGROUND: Exposure to excessive heat can impact kidney health. Climate change is projected to aggravate this impact. An analysis of articles published between 1958 and 2021 was conducted to explore the progress of the research on this issue. METHODS: This study included a bibliometric analysis wherein Web of Science was used to generate a list of all published articles related to the impact of heat on kidney health. Basic information about the articles, such as titles, authors' names, keywords, and citations, were recorded and analyzed. RESULTS: A total of 226 published articles related to the impact of heat on kidney health were identified as of November 20, 2021. Most of these articles (93%) were published within the last decade. The United States was the most prominent country in terms of research productivity and collaboration. Researchers from the United States were well represented among the top 20 contributors of published articles on the study issue. The productivity of the top 20 authors varied between 6 and 32 articles each. A total of 25 common words used by the authors were identified. The most frequently used keywords were chronic kidney disease, heat stress, acute kidney injury, Mesoamerican nephropathy, and climate change. Keyword analysis revealed 3 distinct major research clusters in the existing scientific research on the impact of heat on kidney health: chronic kidney disease of unknown etiology, heat stress and renal physiology, and the effect of climate change on kidney health. CONCLUSIONS: Research on heat-related kidney injury has witnessed rapid development in recent decades, motivated by the emergence of chronic kidney disease of unknown etiology and climate change. Developing countries in hot regions must increase their productivity in this research area through international collaboration and partnerships.

Developmental lead (Pb)-induced deficits in hippocampal protein translation at the synapses are ameliorated by ascorbate supplementation.

BACKGROUND: Lead (Pb) is a persistent environmental neurotoxin and its exposure even in minute quantities has been known to induce neuronal defects. The immature brain is singularly sensitive to Pb neurotoxicity, and its exposure during development has permanent detrimental effects on the brain developmental trajectory and neuronal signaling and plasticity, culminating into compromises in the cognitive and behavioral attributes which persists even later in adulthood. Several molecular pathways have been implicated in the Pb-mediated disruption of neuronal signaling, including elevated oxidative stress, alterations in neurotransmitter biology, and mitochondrial dysfunction. Nevertheless, the neuronal targets and biochemical pathways underlying these Pb-mediated alterations in synaptic development and function have not been completely deduced. In this respect, recent studies have shown that synaptic signaling and its maintenance and plasticity are critically dependent on localized de novo protein translation at the synaptic terminals. MATERIALS AND METHODS: The present study hence aimed to assess the alterations in the synapse-specific translation induced by developmental Pb exposure. To this end, in vitro protein translation rate was analyzed in the hippocampal synaptoneurosomal fractions of rat pups pre- and postnatally exposed to Pb using a puromycin incorporation assay. Moreover, we evaluated the therapeutic effects of ascorbic acid supplementation against Pb-induced deficits in synapse-localized protein translation. RESULTS: We observed a significant loss in the rates of de novo protein translation in synaptoneurosomes of Pb-exposed pups compared to age-matched control pups. Interestingly, ascorbate supplementation lead to an appreciable recovery in Pb-induced translational deficits. Moreover, the deficit in activity-dependent synaptic protein translation was found to correlate significantly with the increase in the blood Pb levels. CONCLUSION: Dysregulation of synapse-localized de novo protein translation is a potentially critical determinant of Pb-induced synaptic dysfunction and the consequent deficits in behavioral, social, and psychological attributes of the organisms. In addition, our study establishes ascorbate supplementation as a key ameliorative agent against Pb-induced neurotoxicity.