- Pathophysiology
- Dysfunctional Mitochondria Clearance in Situ: Mitophagy in Obesity and Diabetes-Associated Cardiometabolic Diseases
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Songling Tang, Di Hao, Wen Ma, Lian Liu, Jiuyu Gao, Peng Yao, Haifang Yu, Lu Gan, Yu Cao
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Diabetes Metab J. 2024;48(4):503-517. Published online February 15, 2024
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DOI: https://doi.org/10.4093/dmj.2023.0213
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 Abstract
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- Several mitochondrial dysfunctions in obesity and diabetes include impaired mitochondrial membrane potential, excessive mitochondrial reactive oxygen species generation, reduced mitochondrial DNA, increased mitochondrial Ca2+ flux, and mitochondrial dynamics disorders. Mitophagy, specialized autophagy, is responsible for clearing dysfunctional mitochondria in physiological and pathological conditions. As a paradox, inhibition and activation of mitophagy have been observed in obesity and diabetes-related heart disorders, with both exerting bidirectional effects. Suppressed mitophagy is beneficial to mitochondrial homeostasis, also known as benign mitophagy. On the contrary, in most cases, excessive mitophagy is harmful to dysfunctional mitochondria elimination and thus is defined as detrimental mitophagy. In obesity and diabetes, two classical pathways appear to regulate mitophagy, including PTEN-induced putative kinase 1 (PINK1)/Parkin-dependent mitophagy and receptors/adapters-dependent mitophagy. After the pharmacologic interventions of mitophagy, mitochondrial morphology and function have been restored, and cell viability has been further improved. Herein, we summarize the mitochondrial dysfunction and mitophagy alterations in obesity and diabetes, as well as the underlying upstream mechanisms, in order to provide novel therapeutic strategies for the obesity and diabetes-related heart disorders.
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Citations
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Giovanna Leite Santos, Ericka Francislaine Dias Costa, Ana Paula Dalla Costa, Ariane Maria Zanesco, Marcela Reymond Simoes, Fábio Rogério, Daniele Masselli Rodrigues Demolin, Claudia Daniele Carvalho Navarro, Lício Augusto Velloso, Annelise Francisco, Rog
Hormone and Metabolic Research.2025; 57(03): 199. CrossRef - Type 3 diabetes and metabolic reprogramming of brain neurons: causes and therapeutic strategies
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Molecular Medicine.2025;[Epub] CrossRef - WIPI1-mediated mitophagy dysfunction in ventricular remodeling associated with long-term diabetes mellitus
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Cellular Signalling.2025; 130: 111663. CrossRef - Aconiti Lateralis Radix Praeparata ameliorates heart failure via PI3K/AKT/Bnip3 pathway
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Frontiers in Pharmacology.2025;[Epub] CrossRef - Mitophagy in the Pathogenesis of Obesity-Associated Cardiovascular Diseases: New Mechanistic and Therapeutic Insights
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Trends in Medical Research.2024; 19(1): 112. CrossRef - A review: Polysaccharides targeting mitochondria to improve obesity
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International Journal of Biological Macromolecules.2024; 277: 134448. CrossRef - Iron chelators as mitophagy agents: Potential and limitations
Tereza Brogyanyi, Zdeněk Kejík, Kateřina Veselá, Petr Dytrych, David Hoskovec, Michal Masařik, Petr Babula, Robert Kaplánek, Tomáš Přibyl, Jaroslav Zelenka, Tomáš Ruml, Martin Vokurka, Pavel Martásek, Milan Jakubek
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- Complications
- Global, Regional, and National Temporal Trends in Incidence for Type 2 Diabetes Mellitus Related Chronic Kidney Disease from 1992 to 2021
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Yu Cao, Huiting Chen, Hui Liu, Hao Wu, Wei Gao
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Received September 26, 2024 Accepted November 21, 2024 Published online March 11, 2025
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DOI: https://doi.org/10.4093/dmj.2024.0593
[Epub ahead of print]
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Abstract
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- Background
Type 2 diabetes mellitus (T2DM) is a major cause of declining renal function.
Methods
Temporal trends in T2DM-related chronic kidney disease (CKD-T2DM) incidence across 204 countries and territories from 1992 to 2021 were analyzed using data from the Global Burden of Disease 2021. The impact of macro-factors (demographic change, age, period, and birth cohort) on CKD-T2DM incidence trends was assessed using decomposition analyses and age-period- cohort modeling, highlighting opportunities to improve incidence and reduce regional disparities.
Results
In 2021, global CKD-T2DM incidence cases reached 2.01 million, a 150.92% increase since 1992, with population growth and aging contributing to 80% of this rise. The age-standardized incidence rate (ASIR) ranged from 15.09 per 100,000 in low sociodemographic index (SDI) regions to 23.07 in high SDI regions. China, India, the United States, and Japan have the most incidence cases, accounted for 69% of incidence cases globally. With 175 countries showing an increasing ASIR trend. Unfavorable trend in ASIR increase were generally found in most high-middle and middle SDI countries, such as China and Mexico (net drift=0.15% and 1.17%, per year). Age-period-cohort analyses indicated a high incidence risk near age 80, with worsening risks for recent periods and birth cohorts, except in high SDI areas.
Conclusion
The CKD-T2DM incidence burden continues to rise globally, with significant variations between countries, posing major global health implications. CKD-T2DM is largely preventable and treatable, warranting greater attention in global health policy, particularly for older populations and in low and middle SDI regions.
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