Smoking Exposure Leads Physiological and Pathological Transfer, Especially in the Elderly

Aging is a physiological process involving progressive impairment of normal functions, due to an increasing vulnerability to injuries, which reduces the ability of the organism to survive. The physiologic changes of the aging cardiac include left ventricular hypertrophy, increased cardiac fibrosis and valve degeneration [1]. However, cardiovascular disease is a major risk factor for aging cause of death. Aging-related cardiac disease changes in cardiac morphology and functions include decreased myocyte numbers, increased myocyte size, increased left ventricular wall thickness, and decreased conduction fiber density, while functional alterations include a decrease in intrinsic contractility, increased myocardial contraction time, decreased myocardial contraction velocity, and increased myocardial stiffness in left ventricular function [2]. Smoking increases arterial stiffness and coronary cardiac disease. Smoking exposure involves the combination of the smoke emitted by the burning end of a tobacco cigarette and the smoke exhaled by the smoker into the environment [3]. Cardiac pathological hypertrophy due to smoking exposure was observed in old-age patients, which leads to left ventricular remodeling and loss of function. Left ventricular hypertrophy is an initial adaptive response [4]. During LVH development, there is an imbalance of progressive remodeling at the cellular level, involving aging cardiomyocytes physiological and pathological disease transfer.

Aging changes of the elderly heart is associated with physiological cardiac hypertrophy, which is expected or normal aging changes, smoking exposure is associated with pathological hypertrophy. Smoking exposure induced age-related cardiac hypertrophy is associated with numerous molecular and biochemical changes [5]. Calcineurin/NFAT is an originally implicated as pathological hypertrophy signaling pathway. Calcineurin/NFAT is regulated by MAPKs cascades mediated directly and indirectly [6]. However, calcineurin/NFAT regulate cardiac hypertrophy is associated with MEK1-ERK1/2 (physiologic) and MEK5/ERK5 (pathologic) signaling pathways [7]. The subclassified branches MEK5/ERK5 pathways have been implicated in pathological hypertrophy regulation in the heart [8]. In addition, MEK1-ERK1/2 regulate myocytes growth and physiological cardiac hypertrophy function [9]. Indeed, age-associated disease underlies much of the physiological deterioration of old age. Distinctions may be made between “physiological aging” and “pathological aging”. The most well recognized risk factor for many chronic diseases in pathological aging. Interactions between the aging process and the agedrelated disease has not been seriously addressed or systematically explained. Aging is an inevitable process of life [10]. Become progressively disorganized and degraded with age occurring as consequence of physiological aging. Aging process can be described as a progressive function (left ventricular hypertrophy to heart failure) decline that lead to the accumulation of errors that damage repair systems and compromise stem cell function [11]. Aging is a human inevitable adaptive response to exhausted cells, while others regard it as a process that starts at conception and continues until death [12]. Consider aging to be a human physiologic change which has the slowly progressive structural changes and loss in body function with age.

Smoking exposure always make human pathological cardiac hypertrophy in this environment in old age. Smoking exposure may stimuli a phase of cardiac hypertrophy, especially in left ventricular individual. Smoking exposure induced cardiac inflammation led to left ventricular pathological hypertrophy remodeling transfer from aging and increases the risk of a cardiovascular event and mortality.

1. Adamson PB (2013) Aging with heart failure: physiological assessments and risk for hospital admission. J Am Coll Cardiol. 61(6): 643-644.
2. Biernacka A, Frangogiannis NG (2011) Aging and cardiac fibrosis. Aging Dis 2(2): 158-173.
3. Ambrose JA, Barua RS (2004) The pathophysiology of cigarette smoking and cardiovascular disease: an update. J Am Coll Cardiol 43(10): 1731- 1737.
4. Bernardo BC, Weeks KL, Pretorius L, McMullen JR (2010) Molecular distinction between physiological and pathological cardiachypertrophy: experimental findings and therapeutic strategies. Pharmacol Ther 128(1): 191-227.
5. Bernhard D, Moser C, Backovic A, Wick G (2007) Cigarette smoke--an aging accelerator? Exp Gerontol 42(3): 160-165.
6. Folkow B (1993) Pathophysiology of hypertension: differences between young and elderly. Drugs 46 Suppl 2: 3-7.
7. Forman DE, Ahmed A, Fleg JL (2013) Heart failure in very old adults. Curr Heart Fail Rep 10(4): 387-400.
8. Hacker TA, McKiernan SH, Douglas PS, Wanagat J, Aiken JM (2006) Age-related changes in cardiac structure and function in Fischer 344xBrown Norway hybrid rats. Am J Physiol Heart Circ Physiol 290(1): H304-H311.
9. Heineke J, Molkentin JD (2006) Regulation of cardiac hypertrophy by intracellular signaling pathways. Nat Rev Mol Cell Biol 7(8): 589-600.
10. Jahangir A, Sagar S, Terzic A (2007) Aging and cardioprotection. J Appl Physiol (1985) 103(6): 2120-2128.
11. Bueno OF, Molkentin JD (2002) Involvement of extracellular signal-regulated kinases 1/2 in cardiac hypertrophy and cell death. Circ Res 91(9): 776-781.
12. Strait JB, Lakatta EG (2012) Aging-associated cardiovascular changes and their relationship to heart failure. Heart Fail Clin 8(1): 143-164.