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Abplanalp, W.

Publications and source records attributed to Abplanalp, W..

2 recordsLinked to original sources

Human heart organoids reveal a regenerative strategy for mitochondrial disease

The human heart is among the most complex tissues to replicate in vitro, with vascular, neuronal, and immune elements shaping its development and function. Here we describe cardiomorphs, self-organising human cardiac organoids that recapitulate the cellular diversity, structural organisation, vascularisation, and innervation of the myocardium and mature along a developmental trajectory from early cardiogenesis to adult tissue. Using patient-derived cardiomorphs, we establish the first three-dimensional human tissue model of Kearns-Sayre syndrome (KSS), a rare mitochondrial disorder characterised by large-scale mtDNA deletions. KSS-cardiomorphs faithfully reproduce disease-associated metabolic, contractile, and ultrastructural hallmarks. Leveraging this platform, we identify Betaxolol, an FDA-approved selective {beta}1-adrenergic antagonist, as a modulator of mitochondrial quality control. Betaxolol increases intracellular oxygenation, selectively eliminates dysfunctional mitochondria via mitophagy, and promotes biogenesis of functional organelles, restoring contractility in KSS tissues. This dual-action, mutation-agnostic mechanism suggests a therapeutic principle with broad relevance to mitochondrial disease, cardiac pathology, and age-associated decline.

cell biology↗

Ageing impairs the neuro-vascular interface in the heart

Aging is a major risk factor for impaired cardiovascular health. The aging myocardium is characterized by electrophysiological dysfunctions such as a reduced heart rate variability. These alterations can be intrinsic within cardiomyocytes, but might be modulated by the cardiac autonomic nervous system, as well1. It is known that nerves align with vessels during development2, but the impact of aging on the cardiac neuro-vascular interface is unknown. Here, we report that aging reduces nerve density specifically in the left ventricle and dysregulates vascular-derived neuro-regulatory genes. Aging leads further to a down-regulation of miR-145 and de-repression of the neuro-repulsive factor Semaphorin-3A. miR-145 deletion increased Sema3a expression and reduced axon density, thus mimicking the observed aged heart phenotype. Removal of senescent cells, which accumulated with chronological age while nerve density declined, rescued from age-induced dennervation, reduced Sema3a expression and preserved heart rate variability. These data suggest that senescence-associated regulation of neuro-regulatory genes contributes to a declined nerve density of the aging heart and thereby to a reduced heart rate variability.

physiology↗