Oxidative stress and inflammation: the root causes of aging DOI Creative Commons
Prasert Sobhon,

Savedvanich Gavin,

Sawaek Weerakiet

et al.

Exploration of Medicine, Journal Year: 2023, Volume and Issue: unknown, P. 127 - 156

Published: April 17, 2023

Oxygen free radicals [reactive oxygen species (ROS)] and nitrogen (RNS)] are generated by mitochondria during adenosine triphosphate synthesis, catalytic activities of cytochrome P450, nicotinamide adenine dinucleotide phosphate oxidases (NOXs), cyclooxygenases, nitric oxide synthases drug catabolism, phagocytosis, acute inflammation. Under normal circumstances, low levels ROS RNS provide redox signalings that control many essential physiological processes. As age progresses increase excessively due to dysfunctional mitochondria, dysregulated NOX, other free-radical generating sources, leading oxidative stress, which causes oxidation denaturation key cellular components including DNA, proteins, lipids, become abnormal, constituting damage-associated molecular pattern (DAMP), recognized as ‘non-self’ immune cells, inflammation is mediated nuclear factor kappa B-inflammasome, p38-c-Jun N-terminal kinase Janus kinase-signal transducer activator transcription pathways. DAMPs continuously released from damaged senescent causing an otherwise normally transient turning into systemic chronic inflammation, the root cause aging age-associated diseases (AADs). Cells restore balance activating erythroid 2-related 2 (Nrf2) pathway induces synthesis release antioxidation molecules enzymes haem oxygenase-1, also inhibits three inflammatory Furthermore, upregulation autophagy (AP) can get rid abnormal molecules, prevent generation DAMPs, attenuate Both AP Nrf2 decrease with age. The upregulations Nrf2, AP, downregulation controlled sensors energy stress levels, i.e., monophosphate-activated protein kinase, silent information regulator 1, Sestrins, well extracellular matrix, while mammalian targets for rapamycin complex a nutrient sensor, act in opposite direction. If these sensor systems becomes dysregulated, process accelerates, risk AADs increases.

Language: Английский

Exercise and tissue fibrosis: recent advances in therapeutic potential and molecular mechanisms DOI Creative Commons
Zheng Zhao, Yongxue Zhu, David Wan

et al.

Frontiers in Endocrinology, Journal Year: 2025, Volume and Issue: 16

Published: March 20, 2025

Tissue fibrosis represents an aberrant repair process, occurring because of prolonged injury, sustained inflammatory response, or metabolic disorders. It is characterized by excessive accumulation extracellular matrix (ECM), resulting in tissue hardening, structural remodeling, and loss function. This pathological phenomenon a common feature the end stage numerous chronic diseases. Despite advent novel therapeutic modalities, including antifibrotic agents, these have only modest efficacy reversing established are associated with adverse effects. In recent years, growing body research has demonstrated that exercise significant benefits potential treatment fibrosis. The anti-fibrotic effects mediated multiple mechanisms, direct inhibition fibroblast activation, reduction expression pro-fibrotic factors such as transforming growth factor-β (TGF-β) slowing collagen deposition. Furthermore, been to assist maintaining dynamic equilibrium repair, thereby indirectly reducing damage can also help maintain balance improving disorders, exerting anti-inflammatory antioxidant effects, regulating cellular autophagy, restoring mitochondrial function, activating stem cell activity, apoptosis, alleviating tissue. paper presents review its underlying mechanisms for range fibrosis, cardiac, pulmonary, renal, hepatic, skeletal muscle. offers valuable reference point non-pharmacological intervention strategies comprehensive fibrotic

Language: Английский

Citations

0

Comparative effects of aerobic and resistance exercise on bile acid profiles and liver function in patients with non-alcoholic fatty liver disease DOI Creative Commons

Jiasen Shi,

Junchao Cui,

Tianlei Zheng

et al.

BMC Gastroenterology, Journal Year: 2025, Volume and Issue: 25(1)

Published: April 10, 2025

Our research aims to explore the effects of different exercise on liver function and bile acid in patients with non-alcoholic fatty disease (NAFLD), identify most beneficial modalities for NAFLD. Participants were randomly divided into four groups: control group, aerobic training resistance combined group. underwent assessments body shape, blood lipid, glucose levels biochemical parameters. Their measured using LC-MS/MS system. Changes these parameters before after intervention differences between groups analyzed. AT group showed significant improvements Additionally, total acids ursodeoxycholic significantly increased. The RT + also shape parameters, but not as pronounced those Aerobic is modality young NAFLD, it improves while reducing lipid levels. Clinical trial number NCT06338449, registered March 22, 2024.

Language: Английский

Citations

0

HIIT versus MICT in MASLD: mechanisms mediated by gut-liver axis crosstalk, mitochondrial dynamics remodeling, and adipokine signaling attenuation DOI Creative Commons
Dehui Deng, Xu Lin, Yufei Liu

et al.

Lipids in Health and Disease, Journal Year: 2025, Volume and Issue: 24(1)

Published: April 16, 2025

Compare the effects of high-intensity interval training (HIIT) and moderate-intensity continuous (MICT) on metabolic dysfunction-associated steatotic liver disease (MASLD), focusing mechanisms by which these two exercise modalities influence gut microbiota structure, bile acid metabolism, intestinal barrier function, as well their regulatory roles in hepatic lipid synthesis oxidative dynamics. Explore synergistic exercise-mediated mitochondrial fusion remodeling leptin signaling, elucidate causal relationship between gut-derived factors reprogramming, reveal potential multi-scale cross-organ dominant exercise, providing a theoretical basis for systematically comparing different modalities. Thirty-two male rats were randomly divided into NFD (n = 8) HFD 24) groups fed normal chow high-fat chow, respectively. After eight weeks, group was three groups: (1) MICT-8; (2) HIIT-8; (3) HFD-8. At end experiment, blood, liver, ileum, skeletal muscle samples collected analysis rats' baseline conditions, pathway microbiota, analyses. Both modes ameliorated dysregulation attenuated pathological progression, insulin resistance, fat accumulation with MASLD. Furthermore, both interventions counteracted HFD-induced dysfunction restored gut-liver axis homeostasis. HIIT MICT also upregulated acid-related gene expression modulated butyrate-producing bacterial taxa, adjusted abundance butyrate-generating bacteria. improved metabolism MASLD difference not statistically significant. It is noteworthy that more effective improving function than (P < 0.001).

Language: Английский

Citations

0

Risks of liver cirrhosis, hepatocellular carcinoma, hepatic-related complications, and mortality in patients with type 2 diabetes in Taiwan DOI
Hua-Fen Chen, Yung-Yueh Chang, Peter Chen

et al.

World Journal of Diabetes, Journal Year: 2025, Volume and Issue: 16(5)

Published: April 24, 2025

BACKGROUND Hepatitis B and C alcoholic liver disease are the principal causes of hepatic-related morbidity mortality. However, evidence associations between diabetes without above risk factors study endpoints is not well understood. In addition, effects associated metabolic dysfunction exercise on hepatic outcomes still clear. AIM To investigate incidence relative hazards cirrhosis liver, hepatocellular carcinoma (HCC), complications mortality in patients with type 2 (T2D) who were nonalcoholic serologically negative for hepatitis Taiwan. METHODS A total 33184 T2D 648746 nondiabetic subjects selected from Taiwan’s adult preventive health care service linked to various National Health Insurance databases, cancer registry, death registry identify HCC, complications, The Poisson assumption Cox proportional hazard regression model used estimate incidences all endpoints, respectively. We also compared stratified by age, sex, dysfunctions, regular subjects. RESULTS Compared subjects, had a significantly greater (6.32 vs 17.20 per 10000 person-years) [adjusted ratio (aHR) 1.45; 95%CI: 1.30-1.62]. aHRs 1.81, 1.87, 2.08, An older male obesity, hypertension, dyslipidemia further increased risks decreased risk, irrespective status. CONCLUSION Patients at mortality, dysfunctions provide additional hazard. Coordinated interprofessional high-risk education, an emphasis importance physical activity, crucial minimizing outcomes.

Language: Английский

Citations

0

Oxidative stress and inflammation: the root causes of aging DOI Creative Commons
Prasert Sobhon,

Savedvanich Gavin,

Sawaek Weerakiet

et al.

Exploration of Medicine, Journal Year: 2023, Volume and Issue: unknown, P. 127 - 156

Published: April 17, 2023

Oxygen free radicals [reactive oxygen species (ROS)] and nitrogen (RNS)] are generated by mitochondria during adenosine triphosphate synthesis, catalytic activities of cytochrome P450, nicotinamide adenine dinucleotide phosphate oxidases (NOXs), cyclooxygenases, nitric oxide synthases drug catabolism, phagocytosis, acute inflammation. Under normal circumstances, low levels ROS RNS provide redox signalings that control many essential physiological processes. As age progresses increase excessively due to dysfunctional mitochondria, dysregulated NOX, other free-radical generating sources, leading oxidative stress, which causes oxidation denaturation key cellular components including DNA, proteins, lipids, become abnormal, constituting damage-associated molecular pattern (DAMP), recognized as ‘non-self’ immune cells, inflammation is mediated nuclear factor kappa B-inflammasome, p38-c-Jun N-terminal kinase Janus kinase-signal transducer activator transcription pathways. DAMPs continuously released from damaged senescent causing an otherwise normally transient turning into systemic chronic inflammation, the root cause aging age-associated diseases (AADs). Cells restore balance activating erythroid 2-related 2 (Nrf2) pathway induces synthesis release antioxidation molecules enzymes haem oxygenase-1, also inhibits three inflammatory Furthermore, upregulation autophagy (AP) can get rid abnormal molecules, prevent generation DAMPs, attenuate Both AP Nrf2 decrease with age. The upregulations Nrf2, AP, downregulation controlled sensors energy stress levels, i.e., monophosphate-activated protein kinase, silent information regulator 1, Sestrins, well extracellular matrix, while mammalian targets for rapamycin complex a nutrient sensor, act in opposite direction. If these sensor systems becomes dysregulated, process accelerates, risk AADs increases.

Language: Английский

Citations

10