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Recent progress in cancer therapy has decreased all-cancer mortality, but cardiovascular adverse events owing to chemotherapy and radiotherapy have greater impact on clinical outcome and quality of life in cancer patients and survivors. There are a wide variety of cardiovascular adverse events related to cancer therapy, and the opportunities requiring specialized care by cardiovascular experts are increasing in clinical practice. Under such circumstances, onco-cardiology is becoming very important as a new discipline and attracting much attention in Japan. The Japanese Onco-Cardiology Society was established in 2017, and continues integration of academic activities to solve challenging problems in this field. Interdisciplinary collaborations between cardiologists and oncologists will be further progressed in medical care, clinical and basic research, and education.

Recent progress in cancer therapy has improved the long-term outcomes of cancer patients, and it has increased the importance of managing cardiovascular complications associated with cancer and cancer therapies. In the field of hematology, there is a serious concern about cardiovascular complications associated with a variety of chemotherapeutic drugs, such as anthracyclines, BCR-ABL tyrosine kinase inhibitors, and proteasome inhibitors. Despite the recent accumulation of epidemiological and clinical data and the fact that these are molecularly targeted drugs, molecular mechanisms underlying the pathogenesis of cardiovascular toxicities associated with individual drugs remain to be precisely defined. Recently emerging "onco-cardiology" will extend the interdisciplinary collaboration between oncology, hematology, and cardiology specialists in clinical practice, research, and education in order to protect cancer patients and survivors from cardiovascular complications.

Recent progress in cancer chemotherapy has improved the long-term outcome for cancer patients. Under such circumstances, it is increasingly of clinical importance to manage the cardiovascular complications, which are related to both cancer itself and adverse effects of cancer therapies. Among the most concerning as cardiovascular complications of cancer therapies is chemotherapy-induced cardiotoxicity or chemotherapy-related cardiac dysfunction(CTRCD). CTRCD has been intuitively classified according to the extent of structural abnormalities and degree of reversibility; type 1 is irreversible and dose-dependent with structural abnormalities, and type 2 is reversible after cessation of treatment and dose-independent without structural abnormalities. An example of drugs causing type 1 and 2 CTRCD is anthracyclines and trastuzumab, respectively, although both drugs are likely to induce cardiotoxicity through a combined action. In addition, there is growing awareness that CTRCD is also caused by anti-VEGF inhibitors and tyrosine kinase inhibitors(TKIs), particularly in patients with cardiovascular comorbidities and risk factors. Interdisciplinary collaboration between oncology and cardiology specialists will contribute to the solution of unmet needs to elucidate epidemiologic and pathophysiologic aspects of CTRCD and to establish diagnostic strategies with risk prediction and evidence-based therapeutic strategies against CTRCD in cancer patients and cancer survivors.

Chronic inflammation is one of the common pathological bases underlying aging and aging-related diseases. Recently, it was reported that complement C1q, a crucial regulator of innate immunity, is deeply involved in the pathogenesis of aging-related sarcopenia, heart failure, and hypertension-induced aortic remodeling. In this review, the role and function of chronic inflammation in aging and aging-related diseases will be summarized.

Why do we age, and how do we age ? There have been more than hundreds of theories of aging that attempt rational explanation for these challenging questions. From an evolu- tionary viewpoint, genetic trade-off between longevity and fecundity could explain the evo- lution of aging. Recent applications of new experimental methods and techniques to aging research provided mechanistic insights into the role of oxidative stress, mitochondrial dys- function, cellular senescence, and modulation of the insulin/insulin-like growth factor sig- naling and NAD+-dependent deacetylase sirtuins in aging process. In this article, a long history of aging research is looked back on, and the concepts and theories of aging are summarized.

Calpains are Ca(2 +) -dependent cysteine proteases. Fifteen gene products of calpains are expressed in mammals. Among them, Calpain 1 and Calpain 2 are ubiquitously expressed and have been investigated extensively. Under the physiological conditions, calpain activity is strictly regulated by endogenous inhibitory protein, Calpastatin. Calpains are activated in the various cardiovascular diseases and implicated in their pathogenesis by degrading numerous target proteins. Here we briefly summarize the physiological and pathological role of calpains in the cardiovascular diseases.

A growing body of evidence indicates that activation of angiotensin II (Ang II) type 1 (AT1) receptor, a seven -transmembrane G protein -coupled receptor, is critically involved in the development of various cardiovascular diseases. Inherently, AT1 receptor is structurally unstable, and shows spontaneous constitutive activity in an Ang II-independent manner. The constitutive activity of AT1 receptor under basal conditions contributes to the cardiac remodeling even in the absence of Ang II, when AT1 receptor is up-regulated in the heart. Furthermore, mechanical stress can activate AT1 receptor by inducing conformational switch without the involvement of Ang II, and induce cardiac hypertrophy in vivo. These agonist-independent activities of AT1 receptor can be inhibited by inverse agonists, but not by neutral antagonists. Therefore, inverse agonism of AT1 receptor blockers provides therapeutic benefits in the prevention of cardiac remodeling, and thus has potential impact on long-term outcomes in patients with cardiovascular diseases.

Pharmacological inhibitions of the renin-angiotensin-aldosterone system (RAAS) are crowned with one of the greatest success in the current field of cardiovascular medicine. In addition to the systemic effects including elevation of blood pressure and retention of sodium and water, sustained and excessive RAAS activation has direct and deleterious effects on a wide variety of tissues. Recent studies have deciphered the regulatory mechanisms underlying tissue RAAS activation at cellular and molecular levels, and suggested pathogenic roles of RAAS activation in hitherto unanticipated disorders such as muscular dystrophy, osteoporosis, cancer, and aging itself. Novel drugs targeting RAAS are under research and development in search for further efficacy, specificity, and even multifunctionality. This review will discuss the current progress and future perspective of RAAS research.

The octapeptide angiotensin II (AngII) plays a homeostatic role in the regulation of blood pressure and water and electrolyte balance, and contributes to the progression of cardiovascular remodeling. AngII activates AngII type 1 (AT1) receptor and type 2 (AT2) receptor, both of which belong to the seven-transmembrane, G protein-coupled receptor family. Most of the actions of AngII such as promotion of cellular proliferation, hypertrophy, and fibrosis are mediated by AT1 receptor. However, in some pathological situations, AT2 receptor showed an increase in expression level and functions to antagonize the actions by AT1 receptor stimulation. Recent studies have advanced our understanding of the molecular mechanisms underlying receptor activation and signal transduction, and elucidated the pathophysiological roles of AT1 and AT2 receptors in the cardiovascular system.

Pharmacological treatment of chronic heart failure has considerably changed according as a shift of the pathophysiological concept. During the past two decades, it became clear that neurohumoral stimulations play an important role in the progression of heart failure by promoting cardiac remodeling. Administration of angiotensin-converting enzyme-inhibitors, angiotensin II receptor blockers, and beta blockers is now an essential treatment that reduces morbidity and mortality. In spite of an increase in available treatments, the prognosis of symptomatic heart failure remains to be poor. To establish newer and successful treatments, further advancement in our understanding of the molecular mechanisms underlying the pathogenesis of heart failure will be required. Currently, several novel approaches are being tested targeting prevention of cardiac remodeling and myocardial dysfunction. Cardiomyocyte protection by hematopoietic cytokines and stem cell-based therapy may have a promising therapeutic potential.

Few reports have discussed the absorbed dose on CT units with increased scanning capacity even with the current widespread adoption of multi-slice CT units. To compare and investigate the dose indexes among CT units, we measured the absorbed dose on CT units operating in Nagano Prefecture Japan. The measurements showed proportionality between phantom absorbed dose and the exposured mAs values in conventional scanning operation. Further, the measurements showed that the absorbed dose in the center of the phantom differed by about 2.1-fold between the highest and lowest levels on individual CT units. Within a single company, multi-slice CT units of the same company gave absorbed doses of about 1.3 to 1.5 times those of conventional single-slice CT units under the same exposured conditions of conventional scanning. When the scanning pitch was reduced in helical scanning, the absorbed dose at the center of the phantom increased.