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When the clinical features of AAwhich vary significantly from one patient to anotherare examined, research has demonstrated that the disease manifests across a broad spectrum

Current mitochondrial therapies under consideration for POAG span a wide degree of interventions, from lifestyle changes to biologic alterations

In a CLP-induced mouse model of AKI, the E3 ligase MDM2 increased the expression of LMNB1 by promoting the ubiquitinated degradation of p53.LMNB1 may promote mitochondrial damage and ferroptosis in renal tubular epithelial cells and be involved in the development of AKI[22]

Astrocytic reactivity reflects activation of complex molecularly defined programmes which define remodelling of biochemical, morphological, metabolic, and physiological properties of astroglia leading to an upregulation or loss of homoeostatic cascades, or in gain of new protective or regenerative functions

The CITIID-NIHR COVID-19 BioResource Collaboration