Inflammation in ischemic stroke patients with type 2 diabetes – Part II: Potential therapeutic targets

Abstract

Stroke is the leading cause of disability and the second leading cause of death worldwide. Diabetes mellitus is a critical independent cardiovascular risk factor in patients, irrespective of age, smoking, and hypertension. Approximately one-third of first-time ischemic stroke patients have diabetes. Inflammation is among the most important pathological mechanisms in atheroma formation, the damage cascades of the acute phase, as well as during the subacute and chronic phases after stroke. Diabetes, as a common risk factor for stroke, is often present for a long time before a stroke occurs, causing low-grade inflammation, and disrupting the proper functioning of the neurovascular units. These proinflammatory processes and maladaptive immune mechanisms are further accelerated after cerebral ischemia and worsen the stroke outcome in diabetic patients. Clinical treatments for ischemic stroke are currently focused on restoring cerebral blood flow (reperfusion) in the acute phase, including thrombolysis and mechanical thrombectomy, which are not applicable to patients that fall outside of the treatment window and/or without large-vessel occlusion. There are few approved treatments targeting cellular injury caused by inflammation. There are even fewer data on effective treatment for diabetic stroke targeting inflammation. This paper presents the first part of a review focusing on the temporospatial aspects of inflammation in ischemic stroke pathophysiology in stroke patients with type 2 diabetes.