Diabetes abolish cardioprotective effects of remote ischemic conditioning: evidences and possible mechanisms

Tyagi, Sonia; Singh, Nirmal; Virdi, Jaspreet; Jaggi, Amteshwar Singh

doi:10.1007/s13105-019-00664-w

Cited by 34 publications

(31 citation statements)

References 68 publications

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“…Numerous studies have reported the efficacy of RIC in patients undergoing heart surgery and the coronary artery disease [60]. Several different cardioprotective mechanisms have been described for RIC [60][61][62][63]. It seems that the three forms of RIC have similar mechanisms (Figure 4).…”

Section: Effects Of Remote Conditioning Protocols In Diabetesmentioning

confidence: 99%

“…In postconditioning RIC (post-RIC), the short cycles of IR are delivered to the remote organ during the heart reperfusion [57][58][59]. Numerous studies have reported the efficacy of RIC in patients undergoing heart surgery and the coronary artery disease [60]. Several different cardioprotective mechanisms have been described for RIC [60][61][62][63].…”

Section: Effects Of Remote Conditioning Protocols In Diabetesmentioning

confidence: 99%

“…Indeed, RIC-protection is abolished in the diabetic animal model, most likely due to the presence of diabetic neuropathy, reducing the functionality of the neural pathway [66,67]. The main mechanisms on how diabetes may impair the cardioprotective effects of RIC have been recently summarized [60]. For instance, the impairment of the cardioprotective humoral factor may contribute in part to attenuating RIC-induced cardioprotection [60].…”

Section: Of 22mentioning

confidence: 99%

“…The main mechanisms on how diabetes may impair the cardioprotective effects of RIC have been recently summarized [60]. For instance, the impairment of the cardioprotective humoral factor may contribute in part to attenuating RIC-induced cardioprotection [60]. In addition, humoral impairment has been linked to diabetic neuropathy [67].…”

Section: Of 22mentioning

confidence: 99%

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Diabetic Cardiomyopathy and Ischemic Heart Disease: Prevention and Therapy by Exercise and Conditioning

Crisafulli

Pagliaro

Roberto

et al. 2020

IJMS

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Metabolic syndrome, diabetes, and ischemic heart disease are among the leading causes of death and disability in Western countries. Diabetic cardiomyopathy is responsible for the most severe signs and symptoms. An important strategy for reducing the incidence of cardiovascular disease is regular exercise. Remote ischemic conditioning has some similarity with exercise and can be induced by short periods of ischemia and reperfusion of a limb, and it can be performed in people who cannot exercise. There is abundant evidence that exercise is beneficial in diabetes and ischemic heart disease, but there is a need to elucidate the specific cardiovascular effects of emerging and unconventional forms of exercise in people with diabetes. In addition, remote ischemic conditioning may be considered among the options to induce beneficial effects in these patients. The characteristics and interactions of diabetes and ischemic heart disease, and the known effects of exercise and remote ischemic conditioning in the presence of metabolic syndrome and diabetes, are analyzed in this brief review.

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Section: Effects Of Remote Conditioning Protocols In Diabetesmentioning

confidence: 99%

Section: Effects Of Remote Conditioning Protocols In Diabetesmentioning

confidence: 99%

Section: Of 22mentioning

confidence: 99%

Section: Of 22mentioning

confidence: 99%

See 2 more Smart Citations

Diabetic Cardiomyopathy and Ischemic Heart Disease: Prevention and Therapy by Exercise and Conditioning

Crisafulli

Pagliaro

Roberto

et al. 2020

IJMS

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“…Diabetes seems to attenuate the cardioprotective effects of pharmacological and ischaemic conditioning manoeuvers . This may partly be because of dysregulation of mitochondrial homeostasis, by impairing autophagy, overproduction of ROS, lipotoxicity and activation of calpain that has been linked to F‐ATPase proteolysis .…”

Section: Challenges In Translating Mitoprotection Into the Clinical Smentioning

confidence: 99%

Translational issues for mitoprotective agents as adjunct to reperfusion therapy in patients with ST‐segment elevation myocardial infarction

Bøtker

Cabrera-Fuentes

Ruiz‐Meana

et al. 2020

J Cellular Molecular Medi

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Pre‐clinical studies have indicated that mitoprotective drugs may add cardioprotection beyond rapid revascularization, antiplatelet therapy and risk modification. We review the clinical efficacy of mitoprotective drugs that have progressed to clinical testing comprising cyclosporine A, KAI‐9803, MTP131 and TRO 40303. Whereas cyclosporine may reduce infarct size in patients undergoing primary angioplasty as evaluated by release of myocardial ischaemic biomarkers and infarct size imaging, the other drugs were not capable of demonstrating this effect in the clinical setting. The absent effect leaves the role of the mitochondrial permeability transition pore for reperfusion injury in humans unanswered and indicates that targeting one single mechanism to provide mitoprotection may not be efficient. Moreover, the lack of effect may relate to favourable outcome with current optimal therapy, but conditions such as age, sex, diabetes, dyslipidaemia and concurrent medications may also alter mitochondrial function. However, as long as the molecular structure of the pore remains unknown and specific inhibitors of its opening are lacking, the mitochondrial permeability transition pore remains a target for alleviation of reperfusion injury. Nevertheless, taking conditions such as ageing, sex, comorbidities and co‐medication into account may be of paramount importance during the design of pre‐clinical and clinical studies testing mitoprotective drugs.

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Atg5 knockdown induces age-dependent cardiomyopathy which can be rescued by repeated remote ischemic conditioning

Wang

Gao

et al. 2021

Basic Res Cardiol

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Altered autophagy is implicated in several human cardiovascular diseases. Remote ischemic conditioning (RIC) is cardioprotective in multiple cardiovascular injury models and modifies autophagy signaling, but its effect in cardiomyopathy induced by gene manipulation has not been reported. To investigate the cardiac effects of chronically reduced autophagy as a result of Atg5 knockdown and assess whether RIC can rescue the phenotype. Atg5 knockdown was induced with tamoxifen for 14 days in cardiac-specific conditional Atg5 flox mice. Autophagy proteins and cardiac function were evaluated by Western blot and echocardiography, respectively. RIC was induced by cyclical hindlimb ischemia and reperfusion using a tourniquet. RIC or sham procedure was performed daily during tamoxifen induction and, in separate experiments, chronically 3 times per week for 8 weeks. Cardiac responses were assessed by end of the study. Cardiac-specific knockdown of Atg5 reduced protein levels by 70% and was associated with a significant increase in mTOR, a reduction of LC3-II and increased upstream autophagy proteins including LC3-I, P62, and Beclin. The changes in biochemical markers were associated with development of an age-related cardiomyopathy during the 17-month follow-up indicated by increased heart weight body weight ratio, progressive decline in cardiac function, and premature death . RIC increased cardiac ATG5 and rescued some of the Atg5 knockdown-induced cardiomyopathy phenotype and associated morphological remodeling. We conclude that cardiac-specific Atg5 knockdown leads to the development of age-related cardiomyopathy. RIC reverses the molecular and structural phenotype when administered both acutely and chronically. Supplementary Information The online version contains supplementary material available at 10.1007/s00395-021-00888-2.

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Diabetes abolish cardioprotective effects of remote ischemic conditioning: evidences and possible mechanisms

Cited by 34 publications

References 68 publications

Diabetic Cardiomyopathy and Ischemic Heart Disease: Prevention and Therapy by Exercise and Conditioning

Diabetic Cardiomyopathy and Ischemic Heart Disease: Prevention and Therapy by Exercise and Conditioning

Translational issues for mitoprotective agents as adjunct to reperfusion therapy in patients with ST‐segment elevation myocardial infarction

Atg5 knockdown induces age-dependent cardiomyopathy which can be rescued by repeated remote ischemic conditioning

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