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已发表论文
高迁移率族蛋白 B1 在衰老特征中的模糊角色：综述性叙述
Authors Ning M, Liang Y , Zhang L, Wang F, He L
Received 30 June 2025
Accepted for publication 3 October 2025
Published 10 October 2025 Volume 2025:20 Pages 1729—1740
DOI https://doi.org/10.2147/CIA.S550572
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 2
Editor who approved publication: Dr Maddalena Illario
Manru Ning,1 Yihuai Liang,1,2 Liu Zhang,2 Feifei Wang,1,2 Li He3
1Yunnan Botanee Bio-Technology Group Co., Ltd, Kunming, Yunnan, 650106, People’s Republic of China; 2Yunnan Characteristic Plant Extraction Laboratory Co., Ltd., Kunming, Yunnan, 650106, People’s Republic of China; 3Department of Dermatology, First Affiliated Hospital of Kunming Medical University, Kunming, Yunnan, 650000, People’s Republic of China
Correspondence: Feifei Wang, Yunnan Botanee Bio-Technology Group Co., Ltd., Kunming, Yunnan, 650106, People’s Republic of China, Email wangfeifei@botanee.com Li He, Department of Dermatology, First Affiliated Hospital of Kunming Medical University, Kunming, Yunnan, 650000, People’s Republic of China, Email drheli2662@126.com
Abstract: Aging is a complex, multifactorial process driven by interconnected biological mechanisms collectively known as the hallmarks of aging, which contribute to functional decline and the onset of age-related diseases. High-mobility group box 1 (HMGB1), a nuclear DNA chaperone and damage-associated molecular pattern (DAMP), plays a pivotal role in regulating these hallmarks through its dual functions: preserving genomic stability within the nucleus and promoting inflammatory responses when released extracellularly. This review examines the multifaceted involvement of HMGB1 in key aging hallmarks, such as genomic instability, telomere attrition, mitochondrial dysfunction, and chronic inflammation among others. Preclinical studies demonstrate that nuclear HMGB1 supports chromatin integrity and DNA repair, whereas its extracellular release triggers TLR4/RAGE signaling pathways, thereby intensifying inflammaging and senescence-associated secretory phenotypes (SASP). Emerging therapeutic approaches—such as HMGB1 inhibitors, neutralizing antibodies, and epigenetic modulators—show potential in restoring genomic homeostasis and mitigating age-related pathologies. Nevertheless, significant challenges remain, including elucidating HMGB1’s roles in nutrient sensing and psychosocial stress, fine-tuning interventions to preserve its nuclear functions while minimizing extracellular toxicity, and establishing efficacy in human clinical settings. Addressing these gaps may position HMGB1 as a promising multifunctional target for delaying aging and translating preclinical findings into clinical applications.
Keywords: aging, HMGB1, hallmarks of aging, preclinical studies
1Yunnan Botanee Bio-Technology Group Co., Ltd, Kunming, Yunnan, 650106, People’s Republic of China; 2Yunnan Characteristic Plant Extraction Laboratory Co., Ltd., Kunming, Yunnan, 650106, People’s Republic of China; 3Department of Dermatology, First Affiliated Hospital of Kunming Medical University, Kunming, Yunnan, 650000, People’s Republic of China
Correspondence: Feifei Wang, Yunnan Botanee Bio-Technology Group Co., Ltd., Kunming, Yunnan, 650106, People’s Republic of China, Email wangfeifei@botanee.com Li He, Department of Dermatology, First Affiliated Hospital of Kunming Medical University, Kunming, Yunnan, 650000, People’s Republic of China, Email drheli2662@126.com
Abstract: Aging is a complex, multifactorial process driven by interconnected biological mechanisms collectively known as the hallmarks of aging, which contribute to functional decline and the onset of age-related diseases. High-mobility group box 1 (HMGB1), a nuclear DNA chaperone and damage-associated molecular pattern (DAMP), plays a pivotal role in regulating these hallmarks through its dual functions: preserving genomic stability within the nucleus and promoting inflammatory responses when released extracellularly. This review examines the multifaceted involvement of HMGB1 in key aging hallmarks, such as genomic instability, telomere attrition, mitochondrial dysfunction, and chronic inflammation among others. Preclinical studies demonstrate that nuclear HMGB1 supports chromatin integrity and DNA repair, whereas its extracellular release triggers TLR4/RAGE signaling pathways, thereby intensifying inflammaging and senescence-associated secretory phenotypes (SASP). Emerging therapeutic approaches—such as HMGB1 inhibitors, neutralizing antibodies, and epigenetic modulators—show potential in restoring genomic homeostasis and mitigating age-related pathologies. Nevertheless, significant challenges remain, including elucidating HMGB1’s roles in nutrient sensing and psychosocial stress, fine-tuning interventions to preserve its nuclear functions while minimizing extracellular toxicity, and establishing efficacy in human clinical settings. Addressing these gaps may position HMGB1 as a promising multifunctional target for delaying aging and translating preclinical findings into clinical applications.
Keywords: aging, HMGB1, hallmarks of aging, preclinical studies