Novel LOX Variants in Five Families with Aortic/Arterial Aneurysm and Dissection with Variable Connective Tissue Findings.
Ilse Van GuchtAlice KrebsovaBirgitte Rode DinessSteven LagaDave AdlamMarlies KempersNilesh J SamaniTom R WebbAnia A BaranowskaLotte Van Den HeuvelMelanie PerikIlse LuyckxNils PeetersPavel VotypkaMilan MacekJosephina A N MeesterLut Van LaerAline VerstraetenBart L LoeysPublished in: International journal of molecular sciences (2021)
Thoracic aortic aneurysm and dissection (TAAD) is a major cause of cardiovascular morbidity and mortality. Loss-of-function variants in LOX, encoding the extracellular matrix crosslinking enzyme lysyl oxidase, have been reported to cause familial TAAD. Using a next-generation TAAD gene panel, we identified five additional probands carrying LOX variants, including two missense variants affecting highly conserved amino acids in the LOX catalytic domain and three truncating variants. Connective tissue manifestations are apparent in a substantial fraction of the variant carriers. Some LOX variant carriers presented with TAAD early in life, while others had normal aortic diameters at an advanced age. Finally, we identified the first patient with spontaneous coronary artery dissection carrying a LOX variant. In conclusion, our data demonstrate that loss-of-function LOX variants cause a spectrum of aortic and arterial aneurysmal disease, often combined with connective tissue findings.
Keyphrases
- copy number
- coronary artery
- extracellular matrix
- pulmonary artery
- low density lipoprotein
- aortic valve
- left ventricular
- genome wide
- heart failure
- magnetic resonance imaging
- transcription factor
- aortic aneurysm
- amino acid
- early onset
- magnetic resonance
- computed tomography
- spinal cord
- case report
- electronic health record