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Background: CI/R, characterized by ischemic injury following abrupt reestablishment of blood flow, can cause oxidative stress, mitochondrial dysfunction, and apoptosis. We used oxygen-glucose deprivation/reoxygenation (OGD/R) induced injury in HT22 and primary mouse cortical neurons (MCN) as a model for CI/R.

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Introduction: Ischemic stroke, an abrupt blockage of artery, accounting for the most cases of stroke, causes high neurological mortality across the world. Recent evidence has uncovered that circular RNAs (circRNAs) highly engage in ischemic stroke-related neuronal injury. This study concentrated on a novel circRNA hsa_circ_0000304 (termed as circCELF1), trying to unveil its role and underlying mechanism in ischemic stroke.

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Prolonged cold ischemia (CI) is a risk factor for acute kidney injury (AKI) after kidney transplantation (KT). AKI is an abrupt and rapid reduction in renal function due to multi-factors, including inflammation, oxidative stress and apoptosis. V-set immunoglobulin-domain-containing 4 (VSIG4) is a B7 family-related protein and specifically expressed in resting tissue-resident macrophages to mediate various cellular events.

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Acute kidney injury (AKI) is a severe kidney disease defined by partial or abrupt loss of renal function. Emerging evidence indicates that non-coding RNAs (ncRNAs), particularly long non-coding RNAs (lncRNAs), function as essential regulators in AKI development. Here we aimed to explore the underlying molecular mechanism of the lncRNA H19/miR-130a axis for the regulation of inflammation, proliferation, and apoptosis in kidney epithelial cells.

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Ischemia-reperfusion (I/R) injury is a kind of the tissue damage caused by an abrupt re-supplying tissue with blood after a period of ischemia or hypoxia. It contributes to a wide range of pathological processes including kidney injury, circulatory arrest, and especially cardiovascular disease. However, the underlying pathological mechanism is not fully elucidated.

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