Hypoxia and Inflammation as a Consequence of β-Fibril Accumulation: A Perspective View for New Potential Therapeutic Targets

Figure 2

Aspects of cardiac amyloidosis with accumulation of mutated transthyretin amyloid (a). The extracellular space (ES) is constantly enlarged increasing the distance between myocardiocytes and vessels (not visible). (b) At TEM, myocardiocytes display mitochondria with various degree of swelling and alteration of cristae; both are early cell reactions to ATP depletion and hypoxia. Sarcomere ultrastructure is still intact.

(a)

(b)