Lithium–sulfur
(Li–S) batteries suffer from sluggish
sulfur redox reactions under high-sulfur-loading and lean-electrolyte
conditions. Herein, a typical Co@NC heterostructure composed of Co
nanoparticles and a semiconductive N-doped carbon matrix is designed
as a model Mott–Schottky catalyst to exert the electrocatalytic
effect on sulfur electrochemistry. Theoretical and experimental results
reveal the redistribution of charge and a built-in electric field
at the Co@NC heterointerface, which are critical to lowering the energy
barrier of polysulfide reduction and Li2S oxidation in
the discharge and charge process, respectively. With Co@NC Mott–Schottky
catalysts, the Li–S batteries display an ultrahigh capacity
retention of 92.1% and a system-level gravimetric energy density of
307.8 Wh kg–1 under high S loading (10.73 mg cm–2) and lean electrolyte (E/S = 5.9 μL mgsulfur
–1) conditions. The proposed Mott–Schottky
heterostructure not only deepens the understanding of the electrocatalytic
effect in Li–S chemistry but also inspires a rational catalyst
design for advanced high-energy-density batteries.
Oxidative stress causes mitochondrial dysfunction and heart failure through unknown mechanisms. Cardiolipin (CL), a mitochondrial membrane phospholipid required for oxidative phosphorylation, plays a pivotal role in cardiac function. The onset of age-related heart diseases is characterized by aberrant CL acyl composition that is highly sensitive to oxidative damage, leading to CL peroxidation and mitochondrial dysfunction. Here we report a key role of ALCAT1, a lysocardiolipin acyltransferase that catalyzes the synthesis of CL with a high peroxidation index, in mitochondrial dysfunction associated with hypertrophic cardiomyopathy. We show that ALCAT1 expression was potently upregulated by the onset of hyperthyroid cardiomyopathy, leading to oxidative stress and mitochondrial dysfunction. Accordingly, overexpression of ALCAT1 in H9c2 cardiac cells caused severe oxidative stress, lipid peroxidation, and mitochondrial DNA (mtDNA) depletion. Conversely, ablation of ALCAT1 prevented the onset of T4-induced cardiomyopathy and cardiac dysfunction. ALCAT1 deficiency also mitigated oxidative stress, insulin resistance, and mitochondrial dysfunction by improving mitochondrial quality control through upregulation of PINK1, a mitochondrial GTPase required for mitochondrial autophagy. Together, these findings implicate a key role of ALCAT1 as the missing link between oxidative stress and mitochondrial dysfunction in the etiology of age-related heart diseases.
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