1.Advances on Exercise-mediated Regulation of Programmed Cell Death in the Management of Sarcopenia
Journal of Sun Yat-sen University(Medical Sciences) 2025;46(5):737-746
With the acceleration of global population aging, sarcopenia, characterized by a progressive loss of skeletal muscle mass, strength, and physical function, has become a major public health issue that seriously threatens the health and quality of life in older adults. The development and progression of sarcopenia involve complex, multi-level, and cross-system cellular and molecular mechanisms. Recent studies have highlighted the central role of programmed cell death (PCD) in maintaining skeletal muscle homeostasis, regulating metabolism, and mediating tissue repair. The classic forms of PCD-apoptosis, autophagy, pyroptosis, and ferroptosis-interact through critical nodes such as reactive oxygen species(ROS) accumulation, mitochondrial dysfunction, and iron homeostasis disruption, ultimately driving muscle fiber loss, functional decline, and chronic inflammation. These processes underpin the pathology of sarcopenia. Exercise, the most effective non-pharmacological intervention to date, has been shown to precisely regulate multiple PCD pathways. It improves muscle mass, strength, and metabolic stability, and delays the progression of sarcopenia. Specifically, appropriate exercise could inhibit excessive apoptosis, activate protective autophagy, alleviate NLRP3 inflammasome-mediated pyroptosis, and suppress ferroptosis by enhancing antioxidant defenses and maintaining iron homeostasis. This review systematically summarizes the roles and mechanisms of apoptosis, autophagy, pyroptosis, and ferroptosis in sarcopenia. It particularly focuses on the molecular targets and physiological effects of exercise-mediated PCD regulation. The aim is to provide theoretical and practical support for developing personalized and precision exercise interventions targeting PCD pathways for the prevention and management of sarcopenia.
2.Protective effects and mechanism of coenzyme Q10 and vitamin C on doxorubicin-induced gastric mucosal injury and effects of intestinal flora
Xiaomeng ZHAO ; Xueke FENG ; Nan YE ; Panpan WEI ; Zhanwei ZHANG ; Wenyu LU
The Korean Journal of Physiology and Pharmacology 2021;25(4):261-272
Doxorubicin (Dox) is widely used to the treatment of cancer, however, it could cause damage to gastric mucosa. To investigate the protective effects and related mechanisms of coenzyme Q10 (CoQ10) and vitamin C (VC) on Dox-induced gastric mucosal injury, we presented the survey of the 4 groups of the rats with different conditions. The results showed Dox treatment significantly induced GES-1 apoptosis, but preconditioning in GES-1 cells with VC or CoQ10 significantly inhibited the Dox-induced decrease and other harm effects, including the expression and of IκKβ, IκBα, NF-κB/p65 and tumor necrosis factor (TNF-α) in GES-1 cells. Moreover, high-throughput sequencing results showed Dox treatment increased the number of harmful gut microbes, and CoQ10 and VC treatment inhibited this effect. CoQ10 and VC treatment inhibits Dox-induced gastric mucosal injury by inhibiting the activation of the IkKB/IκBα/NF-κB/p65/TNF-α pathway, promoting anti-inflammatory effects of gastric tissue and regulating the composition of the intestinal flora.
3.Protective effects and mechanism of coenzyme Q10 and vitamin C on doxorubicin-induced gastric mucosal injury and effects of intestinal flora
Xiaomeng ZHAO ; Xueke FENG ; Nan YE ; Panpan WEI ; Zhanwei ZHANG ; Wenyu LU
The Korean Journal of Physiology and Pharmacology 2021;25(4):261-272
Doxorubicin (Dox) is widely used to the treatment of cancer, however, it could cause damage to gastric mucosa. To investigate the protective effects and related mechanisms of coenzyme Q10 (CoQ10) and vitamin C (VC) on Dox-induced gastric mucosal injury, we presented the survey of the 4 groups of the rats with different conditions. The results showed Dox treatment significantly induced GES-1 apoptosis, but preconditioning in GES-1 cells with VC or CoQ10 significantly inhibited the Dox-induced decrease and other harm effects, including the expression and of IκKβ, IκBα, NF-κB/p65 and tumor necrosis factor (TNF-α) in GES-1 cells. Moreover, high-throughput sequencing results showed Dox treatment increased the number of harmful gut microbes, and CoQ10 and VC treatment inhibited this effect. CoQ10 and VC treatment inhibits Dox-induced gastric mucosal injury by inhibiting the activation of the IkKB/IκBα/NF-κB/p65/TNF-α pathway, promoting anti-inflammatory effects of gastric tissue and regulating the composition of the intestinal flora.
4. Awareness, treatment and control of hypertension in 640 000 adults in eastern China
Xiaofang YAN ; Jingwei YANG ; Xueke BAI ; Haoran WANG ; Fang FENG ; Libo HOU ; Ying SUN ; Wenjuan WANG ; Xi LI
Chinese Journal of Epidemiology 2020;41(1):68-73
Objective:
To understand the awareness, treatment, and control of hypertension in residents aged 35-75 years in eastern China, analyze the treatment mode for antihypertensive agents while identifying those factors affecting awareness, treatment and control.
Methods:
The data collected in eastern China from the China Patient-Centered Evaluative Assessment of Cardiac Events (PEACE) Million Persons Project were used to obtain the information about the awareness, treatment and control of hypertension in the residents and the antihypertensive medication treatment mode in this area. Multilevel mixed-effects model was used to explore the association of the demographic characteristics of hypertension patients with the rates of awareness, treatment and control of hypertension.
Results:
A total of 640 539 participants aged 35-75 years, mean age (56.9±9.6) years, were included in the analysis, women accounted for 59.7

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