Ruhan Zhang

Hunan University of Traditional Chinese Medicine

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Mi Liu

Hunan University of Traditional Chinese Medicine

Peicheng Lu

Hunan University of Traditional Chinese Medicine

Jie Zhou

Hunan University of Traditional Chinese Medicine

Liang Peng

China-Japan Friendship Hospital

Bo Huang

Hunan University of Traditional Chinese Medicine

Xuan Xu

Hunan University of Traditional Chinese Medicine

Qianyan Liu

Hunan University of Traditional Chinese Medicine

Luo Rong

Hunan University

Weiai Liu

Hunan University of Traditional Chinese Medicine

S. Moy

Argonne National Laboratory

Cooperative Institutions

Hunan University of Traditional Chinese Medicine

Argonne National Laboratory

Joint Center for Structural Genomics

Hunan University

Chinese Academy of Medical Sciences & Peking Union Medical College

Nanjing University of Chinese Medicine

Second Affiliated Hospital of Hunan University of Traditional Chinese Medicine

Nagoya University

Education Department of Hunan Province

Chengdu Medical College

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The Role of Gut Microbiota-Derived Trimethylamine N-Oxide in the Pathogenesis and Treatment of Mild Cognitive Impairment

International Journal of Molecular Sciences (2025)

Haihua Xie Jia‐Qian Jiang Sihui Cao Xuan Xu Jie Zhou

Mild cognitive impairment (MCI) represents a transitional stage between normal aging and dementia, often considered critical for dementia prevention. Despite its significance, no effective clinical treatment for MCI has yet been established. Emerging evidence has demonstrated a strong association between trimethylamine-N-oxide (TMAO), a prominent metabolite derived from the gut microbiota, and MCI, highlighting its potential as a biomarker and therapeutic target. TMAO has been implicated in increasing MCI risk through its influence on factors such as hypertension, cardiovascular disease, depression, diabetes, and stroke. Moreover, it contributes to MCI by promoting oxidative stress, disrupting the blood–brain barrier, impairing synaptic plasticity, inducing inflammation, causing mitochondrial metabolic disturbances, and facilitating abnormal protein aggregation. This review further explores therapeutic strategies targeting TMAO to mitigate MCI progression.

Trimethylamine N-oxide

Pathogenesis

Cognitive Decline

Stroke

Depression

10.3390/ijms26031373

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Crystal structure of a domain of the outer membrane lipoprotein Omp28 from Porphyromonas gingivalis

Ruhan Zhang C. Hatzos S. Moy A. Joachimiak

10.2210/pdb2r2c/pdb

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The crystal structure of the acyl-CoA dehydrogenase family protein from Porphyromonas gingivalis

Ruhan Zhang L. Bigelow J. Abdullah A. Joachimiak

10.2210/pdb2oku/pdb

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Gut microbial metabolites in MASLD: Implications of mitochondrial dysfunction in the pathogenesis and treatment

Hepatology Communications (2024)

Ruhan Zhang Zhaobo Yan Huan Zhong Luo Rong Weiai Liu

With an increasing prevalence, metabolic dysfunction-associated steatotic liver disease (MASLD) has become a major global health problem. MASLD is well-known as a multifactorial disease. Mitochondrial dysfunction and alterations in the gut bacteria are 2 vital events in MASLD. Recent studies have highlighted the cross-talk between microbiota and mitochondria, and mitochondria are recognized as pivotal targets of the gut microbiota to modulate the host's physiological state. Mitochondrial dysfunction plays a vital role in MASLD and is associated with multiple pathological changes, including hepatocyte steatosis, oxidative stress, inflammation, and fibrosis. Metabolites are crucial mediators of the gut microbiota that influence extraintestinal organs. Additionally, regulation of the composition of gut bacteria may serve as a promising therapeutic strategy for MASLD. This study reviewed the potential roles of several common metabolites in MASLD, emphasizing their impact on mitochondrial function. Finally, we discuss the current treatments for MASLD, including probiotics, prebiotics, antibiotics, and fecal microbiota transplantation. These methods concentrate on restoring the gut microbiota to promote host health.

Steatosis

Pathogenesis

Fecal bacteriotherapy

10.1097/hc9.0000000000000484

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Citations (6)