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      <abstractText>Preconditioning, postconditioning and remote conditioning of the myocardium enhance the ability of the heart to withstand a prolonged ischemia/reperfusion insult and the potential to provide novel therapeutic paradigms for cardioprotection. While many signaling pathways leading to endogenous cardioprotection have been elucidated in experimental studies over the last 30 years, no cardioprotective drug is on the market yet for that indication. One likely major reason for this failure to translate cardioprotection into patient benefit is the lack of rigorous and systematic preclinical evaluation of promising cardioprotective therapies prior to their clinical evaluation, since ischemic heart disease in humans is a complex disorder caused by or associated with cardiovascular risk factors and comorbidities. These risk factors and comorbidities induce fundamental alterations in cellular signaling cascades that affect the development of ischemia/reperfusion injury and responses to cardioprotective interventions. Moreover, some of the medications used to treat these comorbidities may impact on cardioprotection by again modifying cellular signaling pathways. The aim of this article is to review the recent evidence that cardiovascular risk factors as well as comorbidities and their medications may modify the response to cardioprotective interventions. We emphasize the critical need for taking into account the presence of cardiovascular risk factors as well as comorbidities and their concomitant medications when designing preclinical studies for the identification and validation of cardioprotective drug targets and clinical studies. This will hopefully maximize the success rate of developing rational approaches to effective cardioprotective therapies for the majority of patients with multiple comorbidities. Significance Statement Ischemic heart disease is a major cause of mortality, however, there are still no cardioprotective drugs on the market. Most studies on cardioprotection have been undertaken in animal models of ischemia/reperfusion in the absence of comorbidities, however, ischemic heart disease develops with other systemic disorders e.g. hypertension, hyperlipidemia, diabetes, atherosclerosis, etc. Here we focus on the preclinical and clinical evidence showing how these comorbidities and their routine medications affect ischemia/reperfusion injury and interfere with cardioprotective strategies.</abstractText>
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;&amp;nbsp;&amp;nbsp;&amp;nbsp;
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							&lt;span class=&quot;author-name&quot; &gt;Botker Hans Erik
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							&lt;span class=&quot;author-name&quot; &gt;Hausenloy Derek J&lt;sup&gt;**&lt;/sup&gt;
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							&lt;span class=&quot;author-name&quot; &gt;Schulz Rainer
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&lt;div class=&quot;title&quot;&gt;&lt;a href=&quot;/gui2/?mode=browse&amp;params=publication;33588788&quot; target=&quot;_blank&quot;&gt;Interaction of Cardiovascular Nonmodifiable Risk Factors, Comorbidities and Comedications With Ischemia/Reperfusion Injury and Cardioprotection by Pharmacological Treatments and Ischemic Conditioning&lt;/a&gt;&lt;/div&gt;    &lt;div&gt;		&lt;span class=&quot;journal-title&quot;&gt;PHARMACOLOGICAL REVIEWS&lt;/span&gt;

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							&lt;a style=&quot;color:blue&quot; title=&quot;36753049&quot; target=&quot;_blank&quot; href=&quot;http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&amp;db=PubMed&amp;list_uids=36753049&amp;dopt=Abstract&quot;&gt;
									PubMed
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	&lt;OnlyViewableByAuthor&gt;&lt;div class=&quot;ratings&quot;&gt;
				&lt;div class=&quot;journal-subject&quot;&gt;Folyóirat szakterülete: Scopus - Molecular Medicine&amp;nbsp;&amp;nbsp;&amp;nbsp;SJR indikátor:&amp;nbsp;D1&lt;/div&gt;
				&lt;div class=&quot;journal-subject&quot;&gt;Folyóirat szakterülete: Scopus - Pharmacology&amp;nbsp;&amp;nbsp;&amp;nbsp;SJR indikátor:&amp;nbsp;D1&lt;/div&gt;
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	&lt;div class=&quot;publication-citation&quot; style=&quot;margin-left: 0.5cm;&quot;&gt;
		&lt;span title=&quot;Nyilvános idézőközlemények összesen, említések nélkül&quot; class=&quot;citingPub-count&quot;&gt;Nyilvános idéző összesen: 138&lt;/span&gt;
		| Független: 106
		| Függő: 32
		| Nem jelölt: 0
		| WoS jelölt: 130 
		|  Scopus jelölt:&amp;nbsp;117 
		|  WoS/Scopus jelölt:&amp;nbsp;133 
		|  DOI jelölt:&amp;nbsp;132 
		
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		&lt;a target=&quot;_blank&quot; href=&quot;/api/publication?cond=citations.related;eq;33588788&amp;sort=publishedYear,desc&amp;sort=title&quot;&gt;
			Idézett közlemények száma: 59
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    &lt;div class=&quot;mtid&quot;&gt;&lt;span class=&quot;long-pub-mtid&quot;&gt;Közlemény: 33588788&lt;/span&gt;
    | &lt;span class=&quot;status-data status-VALIDATED&quot;&gt; 	Egyeztetett
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Forrás	 Idéző
	
	
    | &lt;span class=&quot;type-subtype&quot;&gt;Folyóiratcikk
			( Összefoglaló cikk
			
			)
		&lt;/span&gt;
      		| &lt;span class=&quot;pub-category&quot;&gt;Tudományos&lt;/span&gt;
	| &lt;span class=&quot;publication-sourceOfData&quot;&gt;RIS-Egyéb&lt;/span&gt;
&lt;/div&gt;

&lt;div class=&quot;funder&quot;&gt; National Heart Program(NVKP-16-1-2016-0017) Támogató: NKFIH,    (Therapeutic Development thematic program of the Semmelweis University)   &lt;/div&gt;
&lt;div class=&quot;lastModified&quot;&gt;Utolsó módosítás: 2025.06.24. 15:33 Tóth-Lipták Péter (SZTE admin5)
&lt;/div&gt;




	&lt;pre class=&quot;comment&quot; style=&quot;margin-top: 0; margin-bottom: 0;&quot;&gt;&lt;u&gt;Megjegyzés&lt;/u&gt;: Export Date: 3 February 2023            
            CODEN: PAREA&lt;/pre&gt;
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