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(Circulation Research. 2006;98:298.)
© 2006 American Heart Association, Inc.

Editorials

A Female Way to Protect the Heart

Say NO to Calcium

Fabio Di Lisa

From the Dipartimento di Chimica Biologica, Università di Padova, Italy.

Correspondence to Prof Fabio Di Lisa, Dipartimento di Chimica Biologica, Università di Padova, Viale G. Colombo 3, I-35121 Padova, Italy. E-mail dilisa@civ.bio.unipd.it

See related article, pages 403–411

Key Words: nitric oxide • calcium • ischemia • gender • S-nitrosylation • calcium

An extract of the first 250 words of the full text is provided, because this article has no abstract.

	Introduction

 
Both clinical and experimental observations support the concept that female hearts are less susceptible to myocardial injury caused by ischemia and reperfusion.^1,2 A large body of evidence indicates that estrogen is involved in gender-related mechanisms of protection. The protective effect of 17-ß-estradiol (E2) administration was described as a reduced extent of necrosis in rabbit hearts undergoing coronary occlusion followed by reperfusion.³ This initial observation, as well as the reduced myocardial injury in female hearts, has been confirmed in different animal species using various experimental protocols.^4–11 Myocardial protection was shown to be associated with activation of estrogen receptors (ER),⁵ and specifically of ER.⁶ Besides the well-established cytosolic/nuclear localization,^12,13 ER, or at least proteins recognized by anti-ER antibodies, have also been detected at the level of plasma membrane and mitochondria.^14–17 However, the lack of a typical transmembrane domain in cytosolic ER casts doubts about these additional membrane receptors.¹⁵ The activated estrogen–receptor complex triggers the synthesis of specific mRNAs and the production of a number of proteins that are responsible for the various effects elicited in the different cell types. Along with these "genomic" effects, additional processes termed "nongenomic" or alternative occur rapidly and independently of protein synthesis.¹⁸

Among the many pathways that can modify the susceptibility to ischemic injury in female hearts, the relevance of nitric oxide (NO) signaling was addressed by Sun et al in this issue of Circulation Research.¹⁹

	Increased NO Formation Underlies Myocardial Protection in Females

 
Previous studies from Murphy’s group investigated gender differences in hearts subjected to ischemia reperfusion (I/R) protocols under conditions having elevated . . . [Full Text of this Article]

Related Article:

Hypercontractile Female Hearts Exhibit Increased S-Nitrosylation of the L-Type Ca²⁺ Channel 1 Subunit and Reduced Ischemia/Reperfusion Injury

Junhui Sun, Eckard Picht, Kenneth S. Ginsburg, Donald M. Bers, Charles Steenbergen, and Elizabeth Murphy
Circ. Res. 2006 98: 403-411. [Abstract] [Full Text] [PDF]

This article has been cited by other articles:

				B. Ostadal, I. Netuka, J. Maly, J. Besik, and I. Ostadalova Gender Differences in Cardiac Ischemic Injury and Protection--Experimental Aspects Experimental Biology and Medicine, September 1, 2009; 234(9): 1011 - 1019. [Abstract] [Full Text] [PDF]