Advancement of epigenetics in stroke

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Advancement of epigenetics in stroke

Jianhua Peng^1,2,3,4, Dipritu Ghosh^2†, Fan Zhang¹, Lei Yang¹, Jinpeng Wu¹, Jinwei Pang¹, Lifang Zhang⁵, Shigang Yin^2,3* and Yong Jiang^1,2,3,5*

• ¹Department of Neurosurgery, The Affiliated Hospital of Southwest Medical University, Luzhou, China
• ²Laboratory of Neurological Diseases and Brain Function, The Affiliated Hospital of Southwest Medical University, Luzhou, China
• ³Institute of Epigenetics and Brain Science, Southwest Medical University, Luzhou, China
• ⁴Academician (Expert) Workstation of Sichuan Province, The Affiliated Hospital of Southwest Medical University, Luzhou, China
• ⁵Sichuan Clinical Research Center for Neurosurgery, The Affiliated Hospital of Southwest Medical University, Luzhou, China

A wide plethora of intervention procedures, tissue plasminogen activators, mechanical thrombectomy, and several neuroprotective drugs were reported in stroke research over the last decennium. However, against this vivid background of newly emerging pieces of evidence, there is little to no advancement in the overall functional outcomes. With the advancement of epigenetic tools and technologies associated with intervention medicine, stroke research has entered a new fertile. The stroke involves an overabundance of inflammatory responses arising in part due to the body’s immune response to brain injury. Neuroinflammation contributes to significant neuronal cell death and the development of functional impairment and even death in stroke patients. Recent studies have demonstrated that epigenetics plays a key role in post-stroke conditions, leading to inflammatory responses and alteration of the microenvironment within the injured tissue. In this review, we summarize the progress of epigenetics which provides an overview of recent advancements on the emerging key role of secondary brain injury in stroke. We also discuss potential epigenetic therapies related to clinical practice.

Introduction

Stroke is one of the main leading causes of death and the first leading cause of disability worldwide (Avan et al., 2019; Collaborators, 2019). Hemorrhagic stroke, including intracerebral hemorrhage (ICH) and subarachnoid hemorrhage (SAH), happens when a blood vessel in the brain bursts or when brain tissue starts to bleed. On the other hand, ischemic stroke (IS) directly results from the disruption of blood supply to the brain and constitutes approximately 85% of all known cases of stroke. After the stroke, injured brain parenchyma initiates biochemical cascades, which include energy failure, ionic pump failure, oxidative damage, cell death, and inflammation, eventually leading to irreversible brain damage (Iglesias-Rey et al., 2022). Additionally, patients surviving stroke may suffer from functional disabilities that might require temporary or lifelong assistance (Aslanyan et al., 2003). Thus, understanding stroke at the molecular level will help researchers to produce key therapeutic strategies to minimize secondary injuries and promotion of neuroprotection associated with stroke (Saini et al., 2021).

Over the past few decades, researchers have advanced in our understanding of the epigenetic mechanisms involved in the central nervous system (CNS) and its role in neuropsychiatric disorders (Szyf, 2015). These epigenetic-related findings also offer the important translational potential for stroke research. Thus, fully understanding the role of epigenetic regulators in the stroke process is crucial to harness the potential of epigenetic therapies. Here, we review three epigenetic mechanisms involved in secondary brain injuries post-stoke: histone modification, DNA-methylation, and RNA modifications. We also discuss the relevant clinical treatment targeting epigenetics and summarize future advancements in this field.

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