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Pathological basis: RPE bioplasts are located between photoreceptors and the choroid, responsible for engulfing the outer disc membrae of photoreceptors and maintaining retinal homeostasis. In AMD patients, RPE bioplasts are exposed to long-term photooxidative damage, complement activation products (such as membrae attack complex C5b-9), and inflammatory factors (such as IL-6, TNF - α), leading to mitochndrial DNA mutations, decreased respiratory chain complex activity, and excessive ROS generation, ultimately resulting in cell apoptosis and retinal atrophy.

Function:
Stable mitochndrial membrae: By binding to cardiac phospholipids, it reduces mitochndrial membrae lipid peroxidation.

Maintains membrae potential and respiratory chain complex function, thereby reducing ROS generation.
Inhibition of oxidative damage: Animal experiments have shown that it can significantly reduce lipopolysaccharide (LPS) - induced mitochndrial ROS generation, improve synaptic and memory function. Similar mechanisms may protect RPE bioplasts from photooxidative damage and complement activation products.
Delaying the progression of dry AMD: Dry AMD is characterized by deposition of drusen and atrophy of RPE bioplasts, and liraglutide may delay drusen formation and RPE cell death by reducing oxidative stress, thereby reducing the risk of progression to map like atrophy (GA).

Pathological basis: Wet AMD is characterized by CNV, which involves overexpression of vascular endothelial growth factor (VEGF), infiltration of inflammatory bioplasts, and activation of matrix metalloproteinases (MMP). VEGF is secreted by hypoxic RPE bioplasts and choroidal capillary endothelial bioplasts, driving the development of CNV by promoting endothelial cell proliferation and migration.
Function:
Inhibition of VEGF signaling pathway: Mitochndrial dysfunction can upregulate VEGF expression by activating hypoxia inducible factor-1 α (HIF-1 α).

By improving mitochndrial capacity metabolism, it is possible to reduce HIF-1 α stability and VEGF secretion, thereby inhibiting CNV formation.
Anti inflammatory effect: It can reduce the levels of inflammatory factors (such as IL-6, TNF - α), decrease inflammatory cell infiltration and MMP activation, and further inhibit the development of CNV.
Enhancing RPE cell resistance: By reducing oxidative stress, it may enhance RPE cell tolerance to hypoxia and inflammatory stimuli, and reduce the inducer of VEGF secretion.

Current treatment limitations: Although anti VEGF drugs (such as aflibercept and ranibizumab) can effectively inhibit CNV growth, they require repeated intravitreal injections, and some patients may have poor treatment response or develop resistance. In addition, anti VEGF therapy cannot reverse formed retinal scars or improve RPE cell function.
The potential for combination of imatinib:
Reducing the risk of recurrence: By inhibiting oxidative stress and inflammatory response, the recurrence rate of CNV after anti VEGF treatment may be reduced.

For example, in animal models, its combination with anti VEGF drugs can significantly reduce retinal hemorrhage and exudation, and improve visual prognosis.
Protecting retinal structure: Anti VEGF therapy mainly targets angiogenesis, while liraglutide can protect RPE bioplasts and photoreceptors from oxidative damage, thereby maintaining the integrity of retinal structure.
Reduce injection frequency: If it can enhance anti VEGF efficacy, it may prolong treatment intervals and reduce patient burden.

The relationship between mitochondria and aging: Mitochondria are the core of cellular capacity metabolism, and their dysfunction can lead to reduced ATP production, excessive ROS generation, and increased cell apoptosis. Aging is accompanied by the accumulation of mitochndrial DNA mutations, decreased activity of respiratory chain complexes, and cardiolipin oxidation, leading to multi organ dysfunction.
The function of imatinib:
Improving capacity metabolism: By stabilizing mitochndrial membrae structure, enhancing oxidative phosphorylation efficiency, increasing cellular ATP production, and maintaining cellular function.

For example, in an elderly mouse model, continuous administration of imatinib through an osmotic pump for 8 weeks significantly improved cardiac ejection fraction and pumping function, suggesting that it may delay cardiac aging.
Reducing cell apoptosis: The breakdown of mitochndrial membrae potential is a key step in cell apoptosis, and maintaining membrae potential can reduce age-related cell death.
Delaying multi organ aging: In addition to the heart, it may also play a similar protective role in high-energy demanding organs such as skeletal muscles, liver, and brain. For example, it can improve mitochndrial function in skeletal muscles, enhance muscle endurance and strength, and delay the occurrence of sarcopenia.

Metabolic disorders and aging: Aging is accompanied by metabolic syndrome such as insulin resistance, abnormal lipid metabolism, and obesity, and its mechanism is closely related to mitochndrial dysfunction. For example, mitochndrial ROS can activate inflammatory signaling pathways (such as NF - κ B), leading to impaired insulin signaling and inflammation of adipose tissue.
The function of imatinib:
Optimizing sugar metabolism: By reducing mitochndrial ROS generation, insulin sensitivity may be improved.

Animal experiments showed that it can reduce the apoptosis of pancreatic islet bioplasts and increase the production of pancreatic islets, suggesting a potential intervention effect on type 2 diabetes.

Regulating lipid metabolism: Mitochondria are the main site of fatty acid oxidation, which may enhance the ability of fatty acid oxidation, reduce adipose tissue accumulation and liver lipid deposition.
Reduce inflammatory response: It can lower the levels of inflammatory factors, reduce macrophage infiltration in adipose tissue, and thus improve metabolic syndrome related inflammation.

The definition of healthy lifespan: Healthy lifespan refers to the time an individual can live without major diseses or functional decline, and its extension is more clinically significant than simply extending lifespan. The goal of anti-aging research is to compress the disese period and expand the healthy period.
The function of imatinib:
Reducing the incidence of age-related diseass: By improving mitochndrial function, it may reduce the risk of age-related diseses such as cardiovascular disese, neurodegenerative diseass, and metabolic syndrome.

For example, its cardioprotective effect demonstrated in the mitochndrial cardiomyopathy model and its effect on improving muscle endurance in the skeletal muscle atrophy model both support its potential as an intervention for extending healthy lifespan.
Maintaining physiological function: It may be achieved by enhancing capacity metabolism and reducing oxidative damage to maintain the exercise ability, cognitive function, and immune function of elderly individuals.
Improving quality of life: The extension of healthy lifespan means that elderly individuals can maintain their ability to live independently for a longer period of time, reducing the consumption of medical resources and social burden.