Identification of Putative Causal Relationships between Blood-Based Biomarkers and Prediabetes-Induced Senescence: A Comprehensive Review

Nonkululeko Avril Mbatha, A. G. Mushebenge, A. Khathi
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Abstract

Prediabetes, a pivotal phase in glucose metabolism between normalcy and diabetes, exerts a profound influence on the aging process and the risk of age-related diseases. This comprehensive review delves into the intricate web of blood-based biomarkers that collectively expedite senescence, marking the transition from a state of health to age-related complications. Key findings underscore the significance of diverse biomarkers, such as telomere length, p16INK4a, senescence-associated secretory phenotype (SASP) factors, DNA methylation clocks, advanced glycation end products (AGEs), inflammatory and oxidative stress markers, circulating hormones, and additional factors such as folate, B12, and osteocalcin. Not only do these biomarkers serve as indicators of senescence but they also actively fuel chronic inflammation, oxidative stress, and metabolic dysregulation, all of which contribute to accelerated aging. The implications of this understanding are profound, as prediabetes emerges as a critical period in an individual’s life, influencing various physiological systems, including the vascular and neural systems, metabolic functions, hormonal regulation, and bone health. Recognizing the profound influence of prediabetes on senescence provides a foundation for personalized intervention strategies to mitigate age-related complications and promote healthy aging. Future research directions call for a more diverse array of biomarkers, the in-depth exploration of their roles, and the development of tailored precision medicine strategies to ensure a holistic understanding and effective management of prediabetes-induced senescence and its implications for aging. This knowledge has far-reaching implications for public health and clinical practice, emphasizing the need for early detection and intervention in prediabetic individuals to enhance the quality of life in an aging population with diverse needs.
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确定血液生物标志物与糖尿病前期诱发衰老之间的推定因果关系:全面综述
糖尿病前期是糖代谢介于正常与糖尿病之间的一个关键阶段,对衰老过程和老年相关疾病的风险有着深远的影响。这篇综述深入探讨了基于血液的生物标志物的复杂网络,它们共同加速了衰老,标志着从健康状态向老年相关并发症的过渡。主要研究结果强调了端粒长度、p16INK4a、衰老相关分泌表型(SASP)因子、DNA甲基化时钟、高级糖化终产物(AGEs)、炎症和氧化应激标志物、循环激素以及叶酸、B12 和骨钙素等其他因子等各种生物标志物的重要性。这些生物标志物不仅是衰老的指标,而且还积极助长慢性炎症、氧化应激和代谢失调,所有这些都会加速衰老。这一认识具有深远的意义,因为糖尿病前期是人一生中的关键时期,会影响各种生理系统,包括血管和神经系统、代谢功能、激素调节和骨骼健康。认识到糖尿病前期对衰老的深远影响,就为采取个性化干预策略以减轻与年龄有关的并发症和促进健康老龄化奠定了基础。未来的研究方向需要更多样化的生物标志物,深入探讨它们的作用,并开发量身定制的精准医疗策略,以确保全面了解和有效管理糖尿病前期诱导的衰老及其对衰老的影响。这些知识对公共卫生和临床实践具有深远影响,强调了对糖尿病前期患者进行早期检测和干预的必要性,以提高具有不同需求的老龄人口的生活质量。
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