These findings further reveal that the underlying nature of the insult to the adult mammalian heart rather than the conserved upregulation of nestin ultimately determines whether activated ventricular fibroblasts contribute to pathological (e.g., reactive fibrosis secondary to hypertension or in the NILV) or physiological (e.g., reparative fibrosis; scar formation) remodeling (Table 1). The gene discussed is NES; the disease is hypertensive disorder.