Systematic review on OCLN in stroke and atherosclerosis highlights regulatory controversies

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Frontiers in Medicine Published May 8, 2026 Medically reviewed May 8, 2026 DOI ↗ By Dr. Amelia Tan, PhD · Internal Medicine & Chronic Disease

Key Takeaway

Consider the controversial evidence on occludin in stroke and atherosclerosis before drawing clinical conclusions.

This is a systematic review examining the occludin gene in the context of ischemic stroke, atherosclerosis, and hypertensive encephalopathy. The authors synthesize existing literature on the gene's role, focusing on its upstream and downstream regulatory networks, tissue-specific expression differences, and potential as a therapeutic target. The review does not report pooled effect sizes or primary outcome data, as the evidence base is qualitative.

A key argument is that the regulatory networks of occludin remain controversial, with conflicting evidence on its function in different tissues. The feasibility of targeting occludin for therapeutic purposes is also debated, with no clear consensus on its clinical utility.

The authors note significant limitations, including the controversial nature of the gene's expression and regulatory mechanisms. The review does not report a study population, sample size, or specific interventions, as these details were not available in the source material.

Practice relevance is not reported, and the authors do not make specific clinical recommendations. The review underscores the need for more research to clarify occludin's role in these conditions before any therapeutic applications can be considered.

Study Details

Study typeMeta analysis

EvidenceLevel 1

PublishedMay 2026

View Original Abstract ↓

Occludin (OCLN), a core transmembrane protein found in tight junctions, plays a key role in cardiovascular homeostasis by maintaining vascular endothelial barrier integrity and regulating intercellular signaling and metabolic activities. Recent evidence indicates that OCLN dysfunction is closely related to the pathological processes of various cardiovascular and cerebrovascular diseases such as ischemic stroke, atherosclerosis, and hypertensive encephalopathy. Its downregulation of expression or structural damage can directly destroy the blood–brain barrier and peripheral vascular barrier and aggravate vascular leakage, inflammatory cell infiltration, and neuronal damage; OCLN regulates the activity of signaling pathways, such as NF-κB and MAPK, through interaction with proteins such as ZO-1 and claudins, affecting inflammatory response, oxidative stress, and cell apoptosis. New evidence further reveals the non-classical function of OCLN in mediating endothelial autophagy, mitochondrial function, and metabolic reprogramming, suggesting the multidimensionality of its mechanism of action. However, the upstream and downstream regulatory networks of OCLN, tissue-specific expression differences, and their feasibility as therapeutic targets remain controversial. This systematic review examines the progress of research on the molecular mechanisms of OCLN in cardiovascular and cerebrovascular diseases, integrating its dual role in barrier damage, inflammatory cascades, and cell death, and explores potential therapeutic strategies targeting OCLN to repair barriers or regulate related signaling pathways to provide new ideas for precise intervention in cardiovascular and cerebrovascular diseases.