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• W4302024325 endingPage "938" @default.
• W4302024325 startingPage "916" @default.
• W4302024325 abstract "The spatiotemporal specificity of myocardial hypoxia-inducible factors (HIFs) appears in response to acute and chronic hypoxia (including degree of hypoxia) and is modulated by distant neurohumoral forces. Further, transitions between HIF-α isoforms in cardiomyocytes may regulate protection from myocardial dysfunction. Disturbances in circadian rhythms are also considered because the spatiotemporal specificity of HIF correlates with the myocardial injury response: shiftwork patients are more likely to have myocardial infarction and possibly a larger infarct size. The therapeutic goal of injured myocardium is to safeguard surviving cardiomyocytes, improve their function, or even stimulate their regenerative potential. Precisely targeted small-molecule candidates for HIF or combinations based on the HIF mechanism may reduce toxicity and increase the efficacy of myocardial protection. Oxygen maintains the homeostasis of an organism in a delicate balance in different tissues and organs. Under hypoxic conditions, hypoxia-inducible factors (HIFs) are specific and dominant factors in the spatiotemporal regulation of oxygen homeostasis. As the most basic functional unit of the heart at the cellular level, the cardiomyocyte relies on oxygen and nutrients delivered by the microvasculature to keep the heart functioning properly. Under hypoxic stress, HIFs are involved in acute and chronic myocardial pathology because of their spatiotemporal specificity, thus granting them therapeutic potential. Most adult animals lack the ability to regenerate their myocardium entirely following injury, and complete regeneration has long been a goal of clinical treatment for heart failure. The precise manipulation of HIFs (considering their dynamic balance and transformation) and the development of HIF-targeted drugs is therefore an extremely attractive cardioprotective therapy for protecting against myocardial ischemic and hypoxic injury, avoiding myocardial remodeling and heart failure, and promoting recovery of cardiac function. Oxygen maintains the homeostasis of an organism in a delicate balance in different tissues and organs. Under hypoxic conditions, hypoxia-inducible factors (HIFs) are specific and dominant factors in the spatiotemporal regulation of oxygen homeostasis. As the most basic functional unit of the heart at the cellular level, the cardiomyocyte relies on oxygen and nutrients delivered by the microvasculature to keep the heart functioning properly. Under hypoxic stress, HIFs are involved in acute and chronic myocardial pathology because of their spatiotemporal specificity, thus granting them therapeutic potential. Most adult animals lack the ability to regenerate their myocardium entirely following injury, and complete regeneration has long been a goal of clinical treatment for heart failure. The precise manipulation of HIFs (considering their dynamic balance and transformation) and the development of HIF-targeted drugs is therefore an extremely attractive cardioprotective therapy for protecting against myocardial ischemic and hypoxic injury, avoiding myocardial remodeling and heart failure, and promoting recovery of cardiac function. a family of dimeric transcription factors composed of combinations of JUN, FOS, ATF, JDP, and MAF. AP-1 components are encoded by immediate-early genes and regulate the later-phase transcriptional program for tumorigenesis and organ maintenance. an L-type calcium channel (LTCC) that controls ICa,L in the ventricular myocardium where it mediates excitation–contraction coupling and Ca2+ induced-Ca2+ release (termed Ca2+ sparks). under prolonged low perfusion, the myocardium reduces energy expenditure and contractile function to resist ischemic injury and improve its survival rate. the inwardly rectifying K+ current IK1 is a crucial predictor of cardiac resting membrane potential and repolarization in the terminal phase of the ventricular action potential. Kir2.x channels support cardiac IK1, and Kir2.1 (encoded by the KCNJ2 gene) contributes more to ventricular cardiomyocytes than Kir2.2. a nonselective pore in the mitochondrial inner membrane that can cause ATP depletion, accelerated generation of reactive oxygen species (ROS), mitochondrial malfunction, and ultimately cell death. a key voltage-gated cardiac sodium channel, encoded by SCN5A, that controls INa and conducts cardiac excitatory electrical impulses and propagation. the cell-membrane NCX maintains Ca2+ homeostasis and controls INa/Ca. transient ischemia of peripheral organs or distal limbs can protect against ischemia/reperfusion (I/R) injury of target organs (e.g., the heart). This intermittent preconditioning can be sustained by daily exposure to hypoxia at atmospheric or low pressure or by multiple cycles of reoxygenation following a few minutes of hypoxia at atmospheric pressure. in RISK pathways, IL-10, PI3K–AKT, and ERK1/2 are elevated in the heart for cardioprotection. Downstream actions of the RISK pathways converge on GSK-3β, whose inhibition precludes MPTP opening. following complete recovery of coronary blood flow after a brief bout of myocardial ischemia, the contractile dysfunction of the myocardium is disproportionately long-lasting (hours to days), but completely reversible. TNF-α, its receptor subtype 2, and STAT3 are expressed in the cardioprotective SAFE system. STAT signaling, although acutely protective, is also engaged in long-term remodeling and malfunction of the heart." @default.
• W4302024325 created "2022-10-06" @default.
• W4302024325 creator A5002110596 @default.
• W4302024325 creator A5011279643 @default.
• W4302024325 creator A5020994192 @default.
• W4302024325 creator A5078784651 @default.
• W4302024325 date "2022-11-01" @default.
• W4302024325 modified "2023-10-01" @default.
• W4302024325 title "Molecular basis and clinical implications of HIFs in cardiovascular diseases" @default.
• W4302024325 cites W1517566797 @default.
• W4302024325 cites W1554617702 @default.
• W4302024325 cites W1571391428 @default.
• W4302024325 cites W1969530780 @default.
• W4302024325 cites W1970600179 @default.
• W4302024325 cites W1972421865 @default.
• W4302024325 cites W1973092951 @default.
• W4302024325 cites W1975550306 @default.
• W4302024325 cites W1978975295 @default.
• W4302024325 cites W1979891446 @default.
• W4302024325 cites W1981721404 @default.
• W4302024325 cites W1983016916 @default.
• W4302024325 cites W1989389858 @default.
• W4302024325 cites W1992389076 @default.
• W4302024325 cites W1994455383 @default.
• W4302024325 cites W1995827055 @default.
• W4302024325 cites W2000457934 @default.
• W4302024325 cites W2003788310 @default.
• W4302024325 cites W2008376250 @default.
• W4302024325 cites W2013871395 @default.
• W4302024325 cites W2018183883 @default.
• W4302024325 cites W2018722597 @default.
• W4302024325 cites W2020897454 @default.
• W4302024325 cites W2027121745 @default.
• W4302024325 cites W2027852965 @default.
• W4302024325 cites W2029754434 @default.
• W4302024325 cites W2029867899 @default.
• W4302024325 cites W2043749692 @default.
• W4302024325 cites W2058021996 @default.
• W4302024325 cites W2070453537 @default.
• W4302024325 cites W2082340620 @default.
• W4302024325 cites W2086421610 @default.
• W4302024325 cites W2087109026 @default.
• W4302024325 cites W2096351503 @default.
• W4302024325 cites W2102140472 @default.
• W4302024325 cites W2103129100 @default.
• W4302024325 cites W2105250121 @default.
• W4302024325 cites W2111559564 @default.
• W4302024325 cites W2118937934 @default.
• W4302024325 cites W2124106739 @default.
• W4302024325 cites W2127622541 @default.
• W4302024325 cites W2129462206 @default.
• W4302024325 cites W2139387872 @default.
• W4302024325 cites W2141102511 @default.
• W4302024325 cites W2143317349 @default.
• W4302024325 cites W2144625075 @default.
• W4302024325 cites W2144662794 @default.
• W4302024325 cites W2148608806 @default.
• W4302024325 cites W2150967559 @default.
• W4302024325 cites W2151087141 @default.
• W4302024325 cites W2153771223 @default.
• W4302024325 cites W2156433522 @default.
• W4302024325 cites W2156679064 @default.
• W4302024325 cites W2163458823 @default.
• W4302024325 cites W2225797143 @default.
• W4302024325 cites W2274830107 @default.
• W4302024325 cites W2298435024 @default.
• W4302024325 cites W2516249919 @default.
• W4302024325 cites W2528861718 @default.
• W4302024325 cites W2530879109 @default.
• W4302024325 cites W2536252358 @default.
• W4302024325 cites W2537243438 @default.
• W4302024325 cites W2542943305 @default.
• W4302024325 cites W2592471774 @default.
• W4302024325 cites W2600229737 @default.
• W4302024325 cites W2610441235 @default.
• W4302024325 cites W2611388044 @default.
• W4302024325 cites W2620561660 @default.
• W4302024325 cites W2621415901 @default.
• W4302024325 cites W2744126034 @default.
• W4302024325 cites W2756359490 @default.
• W4302024325 cites W2763979809 @default.
• W4302024325 cites W2767490296 @default.
• W4302024325 cites W2787814498 @default.
• W4302024325 cites W2790581905 @default.
• W4302024325 cites W2793324553 @default.
• W4302024325 cites W2796544636 @default.
• W4302024325 cites W2796944579 @default.
• W4302024325 cites W2799410199 @default.
• W4302024325 cites W2800823836 @default.
• W4302024325 cites W2803455900 @default.
• W4302024325 cites W2804936789 @default.
• W4302024325 cites W2807291844 @default.
• W4302024325 cites W2807588107 @default.
• W4302024325 cites W2808020051 @default.
• W4302024325 cites W2849197408 @default.
• W4302024325 cites W2885879668 @default.
• W4302024325 cites W2887191177 @default.
• W4302024325 cites W2900639426 @default.

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