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Review 2025 · 30 atıf

Pharmacological approaches to enhance mitochondrial biogenesis: focus on PGC-1Α, AMPK, and SIRT1 in cellular health

Palabiyik, Ahmet Alperen, Palabiyik, Esra

Özet

BackgroundMitochondrial biogenesis is essential for cellular energy balance and metabolic stability. Its dysregulation is linked to various metabolic and neurodegenerative diseases, making it a significant therapeutic target. Pharmacological approaches aimed at enhancing mitochondrial function have gained attention for their potential to restore cellular metabolism.ObjectivesThis review examines recent advancements in pharmacological strategies targeting mitochondrial biogenesis, focusing on the roles of PGC-1 alpha, AMPK, and SIRT1, alongside novel therapeutic agents and drug delivery systems.MethodsA systematic review of studies published between 2018 and 2023 was conducted using databases such as PubMed, Web of Science, and Elsevier. Keywords related to mitochondrial biogenesis and pharmacological modulation were used to identify relevant literature.ResultsVarious pharmacological agents, including resveratrol, curcumin, and metformin, activate mitochondrial biogenesis through different pathways. SIRT1 activators and AMPK agonists have shown promise in improving mitochondrial function. Advances in mitochondria-targeted drug delivery systems enhance therapeutic efficacy, yet challenges remain in clinical translation due to the complexity of mitochondrial regulation.ConclusionPharmacological modulation of mitochondrial biogenesis holds therapeutic potential for metabolic and neurodegenerative diseases. While preclinical studies are promising, further research is needed to optimize drug efficacy, delivery methods, and personalized treatment strategies.

Anahtar Kelimeler
Mitochondrial biogenesis PGC-1 alpha AMPK SIRT1 Mitochondrial dysfunction DYSFUNCTION
WoS Kategorileri
Biochemistry & Molecular Biology
Sürdürülebilir Kalkınma Amaçları
Künye
Dergi
MOLECULAR BIOLOGY REPORTS
Yıl
2025
Cilt
52
Sayı
1
ISSN
0301-4851
eISSN
1573-4978
DOI
10.1007/s11033-025-10368-8
WoS UID
WOS:001434940400002
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