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Mitochondria are eukaryotic cellular organelles that are known to produce energy through a process called oxidative phosphorylation. Besides their primary function, mitochondria are involved in various cellular processes, including cell growth, differentiation, signaling, metabolism, and senescence. Age-related changes cause a decline in mitochondrial quality and integrity due to increased mitochondrial mutations and oxidative damage. Thus, aging can severely impact mitochondrial functions,...
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The mitochondrial electron transport chain (ETC) is the main energy generation system in the eukaryotic cells. However, mitochondria also produce cytotoxic reactive oxygen species (ROS) due to the large electron flow during oxidative phosphorylation. While Complex I is one of the primary sources of superoxide radicals, ROS production by Complex II is uncommon and may only be observed in cancer cells with mutated complexes.
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Rapidly dividing tumors, embryos, and wounded tissues require more oxygen than usual, lowering the oxygen concentration in the blood. At low oxygen or hypoxic conditions, an oxygen-sensitive transcription factor called the hypoxia-inducible factor 1 or HIF1 is activated. HIF1 is a dimeric protein of alpha (ɑ) and beta (β) subunits.  Under optimal oxygen conditions, HIF1β is present in the nucleus while HIF1ɑ remains in the cytosol. HIF1ɑ is hydroxylated by prolyl...
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Several body functions deteriorate with age. The external signs of aging are easily identifiable. For example, the skin becomes dry, less elastic, and thins out, forming wrinkles. The skin of the face begins to appear looser due to a decrease in the levels of elastic and collagen fibers in the connective tissue. Additionally, melanin production in the hair follicle decreases with age, resulting in gray hair. Moreover, the senses of sight and hearing decline, so glasses and hearing aids may...
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Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...
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Aging is a complex biological phenomenon influenced by various processes that affect cellular and systemic functions. Several prominent theories attempt to explain its mechanisms, highlighting cellular limitations, oxidative damage, and hormonal changes as central factors in aging.
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Related Experiment Video

Updated: Jan 19, 2026

Protection of H9c2 Myocardial Cells from Oxidative Stress by Crocetin via PINK1/Parkin Pathway-Mediated Mitophagy
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SRC suppression attenuates vascular aging by activating FUNDC1-dependent mitophagy.

Linghuan Wang1, Yan Ma2, Tianhu Wang2

  • 1Department of Medicine School, Nankai University, Tianjin 300071, China; Institute of Geriatric Medicine, National Clinical Research Centre for Geriatric Diseases, National Key Lab for Chronic Kidney Disease, Second Medical Centre of Chinese PLA General Hospital, Beijing 100853, China.

Mechanisms of Ageing and Development
|January 17, 2026
PubMed
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SRC, a stress-responsive tyrosine kinase, regulates mitophagy and vascular aging. Inhibiting SRC may offer therapeutic benefits against vascular senescence and atherosclerosis by improving mitochondrial function.

Keywords:
AutophagyFUNDC1Mitochondrial dysfunctionSRCVascular aging

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Area of Science:

  • Vascular Biology
  • Cellular Senescence
  • Mitochondrial Dynamics

Background:

  • Vascular smooth muscle cell senescence drives vascular remodeling and atherosclerosis.
  • Mitochondrial dysfunction and impaired mitophagy are key contributors to vascular aging.
  • The role of SRC (a stress-responsive tyrosine kinase) in vascular aging is not well understood.

Purpose of the Study:

  • To investigate the role of SRC in regulating autophagy and mitophagy in vascular aging.
  • To explore the SRC-FUNDC1 axis in the context of vascular senescence.
  • To evaluate SRC inhibition as a potential therapeutic strategy for vascular aging and atherosclerosis.

Main Methods:

  • Established accelerated vascular aging models in ApoE-/- mice and induced senescence in mouse aortic vascular smooth muscle cells (MOVASs).
  • Utilized pharmacological SRC inhibition (KX2-391) and genetic manipulation (SRC knockdown/overexpression).
  • Assessed mitophagy flux, mitochondrial morphology, senescence markers, and atherosclerotic plaque characteristics.

Main Results:

  • Elevated SRC expression and activity were observed in both in vitro and in vivo vascular aging models.
  • SRC inhibition partially reversed vascular aging features, improved mitochondrial morphology, and reduced atherosclerotic burden.
  • SRC regulates mitophagy via phosphorylation of FUNDC1 (at Tyr18), and this axis is crucial for SRC-mediated protection against senescence.

Conclusions:

  • The SRC-FUNDC1 axis is a critical regulator of mitophagy and vascular aging.
  • SRC inhibition demonstrates therapeutic potential for mitigating vascular senescence and atherosclerosis.
  • Targeting SRC offers a promising avenue for treating age-related vascular diseases.