Molecular Mechanism Analysis of Ischemia-Reperfusion Injury

Ischemia-reperfusion injury (IRI) is a common feature of ischemic stroke and occurs when blood supply is restored after a period of ischemia. Ischemia-reperfusion injury involves a variety of pathological processes such as cellular cell death (apoptosis, necrosis, and ferroptosis), oxidative stress, inflammatory response, blood-brain barrier (BBB) disruption, extracellular matrix (ECM) remodeling, angiogenesis, cardiomyocyte hypertrophy, and fibrosis. With recent advances in endovascular therapies, including thrombectomy and thrombus disruption, reperfusion injury has become an increasing challenge in stroke treatment. Therefore, understanding the mechanisms of cerebral ischemia-reperfusion injury is crucial for the development of effective therapies.

Fig. 1. The intricate signaling network in ischemia-reperfusion (I/R) injury pathogenesis. (Zhang et al., 2024)

Our Services

Ace Therapeutics provides comprehensive pathophysiological mechanism analysis services for cerebral ischemia-reperfusion injury. Our team of highly skilled experts utilizes advanced technologies to help clients study the molecular mechanisms of cerebral ischemia/reperfusion injury and develop potential therapeutic strategies for ischemic stroke.

We conduct carefully designed basic studies to elucidate the mechanisms of ischemia/reperfusion injury.

Service Options	Service Details
Analysis of Oxidative Stress	Superoxide dismutase (SOD) deficient mouse model of cerebral ischemia-reperfusion NADPH oxidase (NOX) gene-deficient MCAO models Superoxide expression and mitochondrial membrane potential (MMP) assays
Analysis of Mitochondrial Autophagy	Mitochondrial dynamics assays Mitochondrial function assays
Analysis of Leukocyte Infiltration-mediated Ischemia-reperfusion Injury	P-selectin Leukocyte β2 integration of CD11a/CD18 Endothelial intercellular adhesion molecule 1 (ICAM-1) α-collagen
Analysis of Platelet-mediated Ischemia-reperfusion Injury	Platelet-derived growth factor (PDGF) Arachidonic acid metabolites Thromboxane A2 Serotonin and platelet factor 4 (PF4)
Analysis of Complement-Mediated Ischemia-Reperfusion Injury	C1q gene The classical complement pathway The alternative pathway The Letin pathway involving MBL/MASP (mannan-binding lectin/mannan-binding lectin-associated serine proteases)
Assessment of BBB Dysfunction	Examination of BBB permeability after ischemia-reperfusion

Therapeutic Strategy Development Services for Ischemia-Reperfusion Injury

In collaboration with leading researchers and pharmaceutical companies, Ace Therapeutics is actively involved in the preclinical development and evaluation of novel therapeutic interventions targeting various mechanisms to limit ischemia-reperfusion-induced brain injury.

Antioxidant therapy: Antioxidants such as iron chelating compounds, catalase, superoxide dismutase, and vitamin E.
Inhibition of leukocyte infiltration: Inhibition of inflammatory factor release, and receptor-mediated leukocyte adhesion to endothelial cells.
Platelet depletion or platelet aggregation inhibition
Complement inhibitors
Post-treatment: Ischemic post-treatment, remote ischemic post-treatment, and pharmacologic post-treatment.

Reference

Zhang, M., et al. (2024). Ischemia-reperfusion injury: molecular mechanisms and therapeutic targets. Signal Transduction and Targeted Therapy, 9(1), 12.

All of our services are intended for preclinical research use only and cannot be used to diagnose, treat or manage patients.

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