EDN1 and cardiac hypertrophy: On one hand, the decrease in glomerular filtration rate and increase in tubular sodium reabsorption due to diabetic nephropathy lead to fluid retention and elevated cardiac preload, directly inducing AHF [28]; on the other hand, the kidneys’ impaired ability to excrete neurohormones leads to abnormally high levels of vasopressin and endothelin-1, aggravating cardiac afterload and promoting myocardial hypertrophy [58,59].