Article

Activation of the protective arm of renin-angiotensin system enhances mitochondrial turnover improving respiration and decreasing integrated stress response in a human Complex III deficiency model

2026-03-23

Abstract excerpt

<h4>ABSTRACT</h4> Primary mitochondrial diseases are clinically and genetically heterogeneous disorders, commonly caused by defects in the oxidative phosphorylation system. This heterogeneity presents major challenges for therapeutic development; however, a shared hallmark across these diseases is the accumulation of dysfunctional mitochondria. Enhancing mitochondrial turnover, by activating the selective degrada...

Topics

Open a Topic to create a Post that cites this publication.

Identifiers and source

Literature Corpus work: 775dd3ae-598a-58af-888b-488392ce8a76
DOI: 10.64898/2026.03.20.711686

Open publication

Related research

Semantic proximity does not establish scientific evidence.

Click a neighbor to travelStep 1 · 12 closest

Activation of the protective arm of renin-angiotensin system enhances mitochondrial turnover improving respiration and decreasing integrated stress response in a human Complex III deficiency modelDOI 10.64898/2026.03.20.711686Read

Mitochondrial Biogenesis as a Pharmacological Target: A New Approach to Acute and Chronic DiseasesSemantic proximity Read

Targeting the Mitochondrial Phenotype in Cockayne Syndrome Patient Cells: From Bioenergetic Fragility to Pharmacologic RescueSemantic proximity Read

Meclizine rescues cardiac function and mitochondrial ultrastructure by ATP- and glycolysis-independent mechanisms in a genetic model of mitochondrial energy dysfunctionSemantic proximity Read

A neuropsychiatric disease-associated mutation in LRRC8B disrupts cellular Ca²⁺ signaling, mitochondrial function, and bioenergeticsSemantic proximity Read

Nix induced mitochondrial fission, mitophagy, and myocyte insulin resistance are abrogated by PKA phosphorylationSemantic proximity Read

Dapagliflozin protects heart function against type-4 cardiorenal syndrome through activation of PKM2/PP1/FUNDC1-dependent mitophagySemantic proximity Read

Inhibition of the ER stress IRE1α inflammatory pathway protects against cell death in mitochondrial complex I mutant cells.Semantic proximity Read

Mitophagy modulation for the treatment of cardiovascular diseasesSemantic proximity Read

FAM210A Regulates Mitochondrial Translation and Maintains Cardiac Mitochondrial HomeostasisSemantic proximity Read

Mutations in DNAJC19 cause altered mitochondrial structure and increased mitochondrial respiration in human iPSC-derived cardiomyocytes.Semantic proximity Read

Cardiomyocyte ATP production, metabolic flexibility, and survival require calcium flux through cardiac ryanodine receptors in vivo.Semantic proximity Read

FAM210A regulates mitochondrial translation and maintains cardiac mitochondrial homeostasisSemantic proximity Read