EDITORIALS

Vitamin D and calcium dyshomoeostasis-associated heart failure

Karl T Weber¹, Robert U Simpson², Laura D Carbone^3,4

¹ Division of Cardiovascular Diseases, University of Tennessee Health Science Center, Memphis, TN, USA
² Department of Pharmacology, University of Michigan Medical School, Ann Arbor, MI, USA
³ Department of Veterans Affairs Medical Center, Memphis, TN
⁴ Division of Connective Tissue Diseases, University of Tennessee Health Science Center, Memphis, TN, USA

Correspondence to:
Professor Karl T Weber, Division of Cardiovascular Diseases, University of Tennessee Health Science Center, 920 Madison Ave, Suite 300, Memphis, TN 38163, USA; KTWeber@utmem.edu

The first 150 words of the full text of this article appear below.

The heart normally is an efficient physiological pump whose muscular compartment is composed of a syncytium of cardiomyocytes nourished by a coronary vasculature and housed within a scaffolding of structural proteins. The contractile properties of cardiomyocytes are governed by the direct interplay between Ca²⁺ and contractile proteins, actin and myosin, and their intracellular handling of Ca²⁺. Likewise, extracellular Ca²⁺ handling, or Ca²⁺ homoeostasis, can indirectly influence cardiomyocyte contractility. Herein, we briefly examine Ca²⁺ dyshomoeostasis and heart failure.

Plasma Ca²⁺ concentrations are highly regulated and maintained within a narrow range. If disturbed, a series of controlling factors and feedback mechanisms are called into play. Overall Ca²⁺ homoeostasis relates to its dietary intake; absorption and excretion from gut and kidneys; bone storage; and the modifying influence of such calcitropic hormones as calcitriol (activated vitamin D) and parathyroid hormone (PTH).

In utero, the availability of Ca²⁺ for fetal growth and development, including . . . [Full text of this article]

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