Autophagy Mechanism Analysis in Stroke

Autophagy is a self-protective cytolytic metabolic pathway through which certain long-lived or misfolded proteins and damaged organelles are degraded into metabolic components and recycled to maintain cellular homeostasis and promote cell survival. Autophagy may induce neuroprotection after ischemic stroke. However, in some specific cases, activation of autophagy can induce cell death and play a deleterious role in the etiology and progression of ischemic stroke. The dual role of autophagy in ischemic stroke may be explained by the involvement of multiple signaling pathways, but the exact role and molecular mechanisms have not been elucidated. Regulation of autophagy has emerged as a potential target for ischemic stroke therapy.

Fig. 1. Schematic illustration of signaling pathways related to autophagy during cerebral ischemia. (Wang et al., 2021)

Our Services

Ace Therapeutics, a leading company in the field of stroke research, provides comprehensive analysis services to study the role of autophagy in stroke, including common signaling pathways and autophagy subtypes (e.g., mitophagy, pexophagy, aggrephagy, endoplasmic reticulum-phagy, and lipophagy). Our team of highly skilled researchers and advanced technologies enable us to provide reliable data to support studies on the exact role and molecular mechanisms of autophagy in ischemic stroke. In addition, we can help clients discover new and effective therapeutic targets for ischemic stroke by modulating autophagy.

We can analyze multiple signaling pathways that play a regulatory role in the formation of autophagy, including but not limited to:

• Mammalian target of rapamycin (mTOR) signaling pathway
• Mitogen-activated protein kinase (MAPK) signaling pathway
• 5'-AMP-activated protein kinase (AMPK) signaling pathway
• Beclin-1 signaling pathway
• Rab7 signaling pathway
• UPR signaling pathway
• HIF-1 signaling pathway

Our Approaches for Monitoring Autophagy After Ischemic Stroke

Detection of autophagic processes and measurement of autophagic activity are essential for studying autophagic function. Our laboratory has a variety of biochemical and cell biological methods for monitoring autophagy to accurately characterize autophagic processes in experimental models of stroke.

LC3 Detection and Quantification

We offer western blotting to quantify LC3 expression levels in animal models of stroke. In addition, we use fluorescence microscopy to track their localization and quantify changes in their distribution and abundance during stroke by labeling LC3 with fluorescent tags. By using cells expressing fluorescently labeled LC3 constructs, we provide flow cytometry to measure the decrease in fluorescence intensity as autophagosomes underwent lysosomal degradation.

Monitoring Selective and Non-selective Autophagy

We offer transmission electron microscopy (TEM) to monitor selective and non-selective autophagy. We can qualitatively and quantitatively analyze a variety of autophagic structural changes to ensure proper identification and quantification of autophagic compartments.

Ace Therapeutics provides comprehensive molecular mechanism analysis services to elucidate the role of autophagy in stroke pathogenesis. Through advanced methodologies and partnerships, we help our clients develop stroke drugs that selectively target autophagy-related signaling pathways. If you are interested in our services, please do not hesitate to contact us!

1. Wang, X., et al. (2021). An updated review of autophagy in ischemic stroke: From mechanisms to therapies. Experimental Neurology, 340, 113684.