Clinical Research in Pulmonology

Current Concept for the Pathogenesis of Idiopathic Pulmonary Fibrosis (IPF)

Review Article | Open Access

  • 1. Department of Medicine, University of Minnesota, Minneapolis, Minnesota 55455, USA
+ Show More - Show Less
Corresponding Authors
Richard Seonghum Nho, 420 Delaware Street SE.Box 276, Minneapolis, Minnesota, 55455, USA, Telephone: 612-625-0686; Fax: 612-625-2174

Nho RS (2013) Current Concept for the Pathogenesis of Idiopathic Pulmonary Fibrosis (IPF). Clin Res Pulmonol 1: 1008.


•    Extracellular matrix
•    Idiopathic pulmonary fibrosis
•    Collagen
•    Integrins


Fibrosis in interstitial lung disease is caused by the accumulation of extracellular matrix proteins within the interstitium and alveolar space of the lung. The majority of severe cases comprise a classification known as idiopathic pulmonary fibrosis (IPF) for which the origin is unknown [1]. IPF is the most severe chronic form of pulmonary fibrosis and results in gradual exchange of normal lung parenchyma with fibrotic tissue and in the irreversible impairment of gas exchange in the lung. IPF is a deadly fibrotic lung disease with a 5 year mortality of 50-70%, comparable to many cancers. The estimated incidence of IPF is 10 per 100,000 individuals with a prevalence of 30 per 100,000 [2]. The current concept for the development of pulmonary fibrosis including IPF is that at least three physiologically balanced processes implicated in the maintenance of lung fibroblasts populations - proliferation, apoptosis of (myo) fibroblasts and production of ECM - are disturbed [3]. Risk factors for IPF include age, male gender and a history of cigarette smoking [4]. A number of genetic mutations such as the surfactant protein C (SFTPC), surfactant protein A2 (SFTPA2) and telomerase (TERT and TERTC) have also been associated with the development of lung fibrosis [5- 7]. IPF is characterized by the accumulation of fibroblasts and collagen within the alveolar wall resulting in obliteration of the gas-exchange surface. Morphological studies have demonstrated that subepithelial accumulation of fibroblasts in a lesion termed the “fibroblastic focus” is the sentinel morphological lesion of IPF [8]. Ultrastructural analysis of the fibroblastic focus has revealed that it is composed of alpha-smooth muscle actin-expressing myofibroblasts enmeshed in a matrix rich in polymerized type I collagen [9]. The key role of the myofibroblast in IPF is established by the observation that progressive expansion of the fibroblastic focus by proliferating myofibroblasts depositing type I collagen leads to permanently scarred alveoli [10-13]. Although this study suggests that myofibroblasts are closely linked to the development of lung fibrosis, the origin of myofibroblasts is still unclear. However, it is speculated that circulating fibrocytes derived from bone marrow, epithelial to mesenchymal transition (EMT) and resident fibroblasts are responsible for the appearance of myofibroblasts [14]. Prior to the activation of myofibroblasts, it is generally believed that an initial or repetitive injury occurs to type I alveolar epithelial cells (AEC-I) which constitute the majority of the alveolar surface [15]. When AEC-I is injured, type II alveolar epithelial cells (AECII) are thought to undergo hyperplastic proliferation and release growth factors, cytokines and other substance that subsequently promote the activation of myofibroblasts, which secret collagen and ECMs. The accumulation of ECM and the hyper-proliferation of myofibroblasts ultimately destroy lung parenchyma. In an effort to elucidate the pathogenesis of this deadly disease, several underlying mechanisms have recently been proposed. One of the critical mechanisms in IPF progression is the physical interaction between ECM and cells. Several cell surface receptors including integrins, discoidin domain receptors (DDRs), syndecans and CD44 have been identified as components of a complex systemresponsible for cell immobilization on normal ECM. Among them, integrins have been extensively studied in IPF fibroblasts. ECM is composed of collagens, elastin, proteoglycans (including hyaluronan) and non-collagenous glycoproteins and forms a complex, three-dimensional network among cells of different tissues in an organ-specific manner and reciprocally influences cellular function to modulate diverse fundamental aspects of cell biology [16,17].

Collagens are the most abundant matrix protein in animal tissues and type I collagen is the major component of ECM in skin, bone, ligamnents, etc. Type I collagen is composed of glycin- and proline rich two-α1 (I) and one-α2 (I) chains [18]. It hasbeen well established that the alteration of integrin function is associated with a pathological IPF fibroblast phenotype. An ECM alteration result from abnormal synthesis or degradation of one or more ECM componentsand contributes to the progression of IPF [19]. Interestingly, there is a sharp difference in proliferation profiles of human lung fibroblasts when they are cultured on 2D and 3D type 1 collagen matrices. Studies showed that tissue culture plates coated with 2D monomeric collagen provide a proliferationpermissive environment for normal and IPF lung fibroblasts [20]. Unlike 2D collagen, 3D matrix, which closely imitates the physiological forms of ECM, is composed of polymerized collagen (fibrillar collagen). Immunohistochemical analysis also revealed that α-smooth muscle actin-expressing myofibroblasts are enmeshed in a type I collagen-rich 3D matrix. Unlike 2D matrix, when normal lung fibroblasts attach to 3D polymerized collagen matrix, cell proliferation is suppressed and apoptosis increases. However, IPF fibroblasts elude the proliferation suppressing and apoptosis inducing effects of polymerized collagen matrix [21,22]. Interestingly, mounting evidence points to similarities between IPF and cancer in some aspects of the IPF phenotype and the underlying disease mechanisms. It is well established that PTEN/PI3K/Akt axis is deregulated in IPF and cancer cells [23-27]. This concept is also supported by other research group’s findings that oncogenic proteins such as Ras and tumor suppressor proteins p53 become abnormally altered, implicating the development of lung carcinoma in IPF patients [28-30]. Thus, these studies strongly suggest that the intrinsic changes of IPF fibroblasts enable them to have a highly proliferative and an apoptosis-resistance phenotype in response to 3D polymerized collagen matrix.

Priorresearch strongly suggest that the understanding the role of cell-ECM interaction is crucial in IPF pathogenesis. This physiological process that accompanies normal wound repair is aberrant in IPF fibroblasts and is mediated by pathological integrin signaling [20]. The α and β chains of integrinscooperate in a specific mode in which the extracellular portion of the α chainis responsible for the ligand-binding specificity of the complex whereasthe intracellular domain of the β chain is associated with the induction of intracellular signaling cascades. Recent studies further revealed that β1 integrin regulates the crucial PTEN/PI3K/Akt axis, thereby altering IPF fibroblast cell phenotype in response to type I collagen matrix [20,21] and this signaling pathway is closely linked to cell proliferation, migration and apoptosis. Thus the precise understanding of the altered PTEN/PI3K/Akt dependent pathway is thought to be vital for the elucidation of IPF pathogenesis.Various profibrotic factors such as TGF-β1, PDGF, ET-1, TNF-α, heat shock protein 47 (HSP47), connective tissue growth factor (CTGF), IL-4, insulinlike growth factor (IGF) and its binding proteins are also known to be associated with the regulation of fibrosis [31]. Furthermore, recent studies suggest epigenetic alterationssuch as DNA methylation, histone modification and microRNAs also contribute the development of IPF. From this concept, the pathological role of DNA methyl transferases (Dnmts), histone acetyltransferases (HATS) and deacetylases (HDACs) havebeen highlighted in the development of lung fibrosis [32-34]. Several miRNAsare known to play a major role of conductors in the pathogenesis of fibrosis [35]. It has been found that about 40 miRNAs have also been linked to fibrosis in various organs and disease settings [36]. Among them, miR155, miR-15b, miR-16, mir21, mir23a, miR26a/b, miR-30c and miR338 are though to be associated with lung fibrosis [36]. However current knowledge about the role of these factors are limited and there should be more future research work needed to establish the pathological function of these regulators in lung fibrosis. Although there has been some progress in understanding the pathogenesis of IPF, the etiology and genesis of IPF remains unknown, and there is still no proven effective therapy available due to the lack of understanding for crucial pathological mechanisms in IPF. Therefore, the precise elucidation of IPF pathogenesis is vital to develop IPF therapy and to further prevent the progression of this deadly disease. In summary, the complexity and heterogeneity exist in IPF studies and the understanding of genetic and epigenetic alterations in the development of lung fibrosis is required for future investigation, and these efforts will ultimately lead to find effective therapeutic targets for the treatment of IPF.


1. Loomis-King H, Flaherty KR, Moore BB. Pathogenesis, current treatments and future directions for idiopathic pulmonary fibrosis. 2013; Curr Opin Pharmacol.13: 377-385.

2. Gay SE, Kazerooni EA, Toews GB, Lynch JP 3rd, Gross BH, Cascade PN, et al. Idiopathic pulmonary fibrosis: predicting response to therapy and survival. 1998; Am J Respir Crit Care Med.157: 1063-1072.

3. Todd NW, Luzina IG, Atamas SP. Molecular and cellular mechanisms of pulmonary fibrosis. 2012; Fibrogenesis Tissue Repair.5: 11.

4. Baumgartner KB, Samet JM, Stidley CA, Colby TV, Waldron JA. Cigarette smoking: a risk factor for idiopathic pulmonary fibrosis. 1997; Am J Respir Crit Care Med.155: 242-248.

5. Thomas AQ, Lane K, Phillips J 3rd, Prince M, Markin C, Speer M, et al. Heterozygosity for a surfactant protein C gene mutation associated with usual interstitial pneumonitis and cellular nonspecific interstitial pneumonitis in one kindred. Am J Respir Crit Care Med. 2002; 165: 1322-8.

6. Wang Y, Kuan PJ, Xing C, Cronkhite JT, Torres F, Rosenblatt RL, et al. Genetic defects in surfactant protein A2 are associated with pulmonary fibrosis and lung cancer. 2009; Am J Hum Genet.84: 52-59.

7. Alder JK, Chen JJ, Lancaster L, Danoff S, Su SC, Cogan JD, et al. Short telomeres are a risk factor for idiopathic pulmonary fibrosis. 2008; Proc Natl Acad Sci U S A.105: 13051-13056.

8. Kuhn C, McDonald JA. The roles of the myofibroblast in idiopathic pulmonary fibrosis. Ultrastructural and immunohistochemical features of sites of active extracellular matrix synthesis. 1991; Am J Pathol.138: 1257-1265.

9. Kuhn C 3rd, Boldt J, King TE Jr, Crouch E, Vartio T, McDonald JA. An immunohistochemical study of architectural remodeling and connective tissue synthesis in pulmonary fibrosis. 1989; Am Rev Respir Dis.140: 1693-1703.

10. Basset F, Ferrans VJ, Soler P, Takemura T, Fukuda Y, Crystal RG. Intraluminal fibrosis in interstitial lung disorders. 1986; Am J Pathol.122: 443-461.

11. Fukuda Y, Ishizaki M, Masuda Y, Kimura G, Kawanami O, Masugi Y. The role of intraalveolar fibrosis in the process of pulmonary structural remodeling in patients with diffuse alveolar damage. 1987; Am J Pathol.126: 171-182.

12. Gay SE, Kazerooni EA, Toews GB, Lynch JP 3rd, Gross BH, Cascade PN, et al. Idiopathic pulmonary fibrosis: predicting response to therapy and survival. 1998; Am J Respir Crit Care Med.157: 1063-1072.

13. Katzenstein AL, Myers JL. Idiopathic pulmonary fibrosis: clinical relevance of pathologic classification. 1998; Am J Respir Crit Care Med.157: 1301-1315.

14. Hinz B, Phan SH, Thannickal VJ, Galli A, Bochaton-Piallat ML, Gabbiani G. The myofibroblast: one function, multiple origins. 2007; Am J Pathol.170: 1807-1816.

15. Günther A, Korfei M, Mahavadi P, von der Beck D, Ruppert C, Markart P. Unravelling the progressive pathophysiology of idiopathic pulmonary fibrosis. 2012; Eur Respir Rev.21: 152-160.

16. Hubmacher D, Apte SS. The biology of the extracellular matrix: novel insights. 2013; Curr Opin Rheumatol.25: 65-70.

17. ynes RO. The extracellular matrix: not just pretty fibrils. 2009; Science.326: 1216-1219.

18. hosh AK. Factors involved in the regulation of type I collagen gene expression: implication in fibrosis. 2002; Exp Biol Med (Maywood).227: 301-314.

19. Lu P, Takai K, Weaver VM, Werb Z. Extracellular matrix degradation and remodeling in development and disease. 2011; Cold Spring Harb Perspect Biol.3.

20. Xia H, Diebold D, Nho R, Perlman D, Kleidon J, Kahm J, et al. Pathological integrin signaling enhances proliferation of primary lung fibroblasts from patients with idiopathic pulmonary fibrosis. 2008; J Exp Med.205: 1659-1672.

21. Nho RS, Hergert P, Kahm J, Jessurun J, Henke C. Pathological alteration of FoxO3a activity promotes idiopathic pulmonary fibrosis fibroblast proliferation on type i collagen matrix. 2011; Am J Pathol.179: 2420- 2430.

22. Koyama H, Raines EW, Bornfeldt KE, Roberts JM, Ross R. Fibrillar collagen inhibits arterial smooth muscle proliferation through regulation of Cdk2 inhibitors. 1996; Cell.87: 1069-1078.

23. Takahashi T, Munakata M, Ohtsuka Y, Nisihara H, Nasuhara Y, Kamachi-Satoh A, et al. Expression and alteration of ras and p53 proteins in patients with lung carcinoma accompanied by idiopathic pulmonary fibrosis. 2002; Cancer.95: 624-633.

24. Kawasaki H, Ogura T, Yokose T, Nagai K, Nishiwaki Y, Esumi H. p53 gene alteration in atypical epithelial lesions and carcinoma in patients with idiopathic pulmonary fibrosis. 2001; Hum Pathol.32: 1043-1049.

25. Vancheri C, Failla M, Crimi N, Raghu G. Idiopathic pulmonary fibrosis: a disease with similarities and links to cancer biology. 2010; Eur Respir J.35: 496-504.

26. Kushibe K, Kawaguchi T, Takahama M, Kimura M, Tojo T, Taniguchi S. Operative indications for lung cancer with idiopathic pulmonary fibrosis. 2007; Thorac Cardiovasc Surg.55: 505-508.

27. Minegishi Y, Sudoh J, Kuribayasi H, Mizutani H, Seike M, Azuma A, et al. The safety and efficacy of weekly paclitaxel in combination with carboplatin for advanced non-small cell lung cancer with idiopathic interstitial pneumonias. 2011; Lung Cancer.71: 70-74.

28. Parsa AT, Holland EC. Cooperative translational control of gene expression by Ras and Akt in cancer. 2004; Trends Mol Med.10: 607- 613.

29. Ozawa Y, Suda T, Naito T, Enomoto N, Hashimoto D, Fujisawa T, et al. Cumulative incidence of and predictive factors for lung cancer in IPF. 2009; Respirology.14: 723-728.

30. Takahashi T, Munakata M, Ohtsuka Y, Nisihara H, Nasuhara Y, Kamachi-Satoh A, et al. Expression and alteration of ras and p53 proteins in patients with lung carcinoma accompanied by idiopathic pulmonary fibrosis. 2002; Cancer.95: 624-633.

31. Razzaque MS, Taguchi T. Pulmonary fibrosis: cellular and molecular events. 2003; Pathol Int.53: 133-145.

32. Bechtel W, McGoohan S, Zeisberg EM, Müller GA, Kalbacher H, Salant DJ, et al. Methylation determines fibroblast activation and fibrogenesis in the kidney. 2010; Nat Med.16: 544-550.

33. Sanders YY, Ambalavanan N, Halloran B, Zhang X, Liu H, Crossman DK, et al. Altered DNA methylation profile in idiopathic pulmonary fibrosis. 2012; Am J Respir Crit Care Med.186: 525-535.

34. Hu B, Gharaee-Kermani M, Wu Z, Phan SH. Epigenetic regulation of myofibroblast differentiation by DNA methylation. 2010; Am J Pathol.177: 21-28.

35. Chau BN, Brenner DA. What goes up must come down: the emerging role of microRNA in fibrosis. 2011; Hepatology.53: 4-6.

36. Vettori S, Gay S, Distler O. Role of MicroRNAs in Fibrosis. 2012; Open Rheumatol J. 6: 130-139.

Received : 22 Jul 2013
Accepted : 31 Jul 2013
Published : 02 Aug 2013
Annals of Otolaryngology and Rhinology
ISSN : 2379-948X
Launched : 2014
JSM Schizophrenia
Launched : 2016
Journal of Nausea
Launched : 2020
JSM Internal Medicine
Launched : 2016
JSM Hepatitis
Launched : 2016
JSM Oro Facial Surgeries
ISSN : 2578-3211
Launched : 2016
Journal of Human Nutrition and Food Science
ISSN : 2333-6706
Launched : 2013
JSM Regenerative Medicine and Bioengineering
ISSN : 2379-0490
Launched : 2013
JSM Spine
ISSN : 2578-3181
Launched : 2016
Archives of Palliative Care
ISSN : 2573-1165
Launched : 2016
JSM Nutritional Disorders
ISSN : 2578-3203
Launched : 2017
Annals of Neurodegenerative Disorders
ISSN : 2476-2032
Launched : 2016
Journal of Fever
ISSN : 2641-7782
Launched : 2017
JSM Bone Marrow Research
ISSN : 2578-3351
Launched : 2016
JSM Mathematics and Statistics
ISSN : 2578-3173
Launched : 2014
Journal of Autoimmunity and Research
ISSN : 2573-1173
Launched : 2014
JSM Arthritis
ISSN : 2475-9155
Launched : 2016
JSM Head and Neck Cancer-Cases and Reviews
ISSN : 2573-1610
Launched : 2016
JSM General Surgery Cases and Images
ISSN : 2573-1564
Launched : 2016
JSM Anatomy and Physiology
ISSN : 2573-1262
Launched : 2016
JSM Dental Surgery
ISSN : 2573-1548
Launched : 2016
Annals of Emergency Surgery
ISSN : 2573-1017
Launched : 2016
Annals of Mens Health and Wellness
ISSN : 2641-7707
Launched : 2017
Journal of Preventive Medicine and Health Care
ISSN : 2576-0084
Launched : 2018
Journal of Chronic Diseases and Management
ISSN : 2573-1300
Launched : 2016
Annals of Vaccines and Immunization
ISSN : 2378-9379
Launched : 2014
JSM Heart Surgery Cases and Images
ISSN : 2578-3157
Launched : 2016
Annals of Reproductive Medicine and Treatment
ISSN : 2573-1092
Launched : 2016
JSM Brain Science
ISSN : 2573-1289
Launched : 2016
JSM Biomarkers
ISSN : 2578-3815
Launched : 2014
JSM Biology
ISSN : 2475-9392
Launched : 2016
Archives of Stem Cell and Research
ISSN : 2578-3580
Launched : 2014
Annals of Clinical and Medical Microbiology
ISSN : 2578-3629
Launched : 2014
JSM Pediatric Surgery
ISSN : 2578-3149
Launched : 2017
Journal of Memory Disorder and Rehabilitation
ISSN : 2578-319X
Launched : 2016
JSM Tropical Medicine and Research
ISSN : 2578-3165
Launched : 2016
JSM Head and Face Medicine
ISSN : 2578-3793
Launched : 2016
JSM Cardiothoracic Surgery
ISSN : 2573-1297
Launched : 2016
JSM Bone and Joint Diseases
ISSN : 2578-3351
Launched : 2017
JSM Bioavailability and Bioequivalence
ISSN : 2641-7812
Launched : 2017
JSM Atherosclerosis
ISSN : 2573-1270
Launched : 2016
Journal of Genitourinary Disorders
ISSN : 2641-7790
Launched : 2017
Journal of Fractures and Sprains
ISSN : 2578-3831
Launched : 2016
Journal of Autism and Epilepsy
ISSN : 2641-7774
Launched : 2016
Annals of Marine Biology and Research
ISSN : 2573-105X
Launched : 2014
JSM Health Education & Primary Health Care
ISSN : 2578-3777
Launched : 2016
JSM Communication Disorders
ISSN : 2578-3807
Launched : 2016
Annals of Musculoskeletal Disorders
ISSN : 2578-3599
Launched : 2016
Annals of Virology and Research
ISSN : 2573-1122
Launched : 2014
JSM Renal Medicine
ISSN : 2573-1637
Launched : 2016
Journal of Muscle Health
ISSN : 2578-3823
Launched : 2016
JSM Genetics and Genomics
ISSN : 2334-1823
Launched : 2013
JSM Anxiety and Depression
ISSN : 2475-9139
Launched : 2016
Clinical Journal of Heart Diseases
ISSN : 2641-7766
Launched : 2016
Annals of Medicinal Chemistry and Research
ISSN : 2378-9336
Launched : 2014
JSM Pain and Management
ISSN : 2578-3378
Launched : 2016
JSM Women's Health
ISSN : 2578-3696
Launched : 2016
Clinical Research in HIV or AIDS
ISSN : 2374-0094
Launched : 2013
Journal of Endocrinology, Diabetes and Obesity
ISSN : 2333-6692
Launched : 2013
Journal of Substance Abuse and Alcoholism
ISSN : 2373-9363
Launched : 2013
JSM Neurosurgery and Spine
ISSN : 2373-9479
Launched : 2013
Journal of Liver and Clinical Research
ISSN : 2379-0830
Launched : 2014
Journal of Drug Design and Research
ISSN : 2379-089X
Launched : 2014
JSM Clinical Oncology and Research
ISSN : 2373-938X
Launched : 2013
JSM Bioinformatics, Genomics and Proteomics
ISSN : 2576-1102
Launched : 2014
JSM Chemistry
ISSN : 2334-1831
Launched : 2013
Journal of Trauma and Care
ISSN : 2573-1246
Launched : 2014
JSM Surgical Oncology and Research
ISSN : 2578-3688
Launched : 2016
Annals of Food Processing and Preservation
ISSN : 2573-1033
Launched : 2016
Journal of Radiology and Radiation Therapy
ISSN : 2333-7095
Launched : 2013
JSM Physical Medicine and Rehabilitation
ISSN : 2578-3572
Launched : 2016
Annals of Clinical Pathology
ISSN : 2373-9282
Launched : 2013
Annals of Cardiovascular Diseases
ISSN : 2641-7731
Launched : 2016
Journal of Behavior
ISSN : 2576-0076
Launched : 2016
Annals of Clinical and Experimental Metabolism
ISSN : 2572-2492
Launched : 2016
Clinical Research in Infectious Diseases
ISSN : 2379-0636
Launched : 2013
JSM Microbiology
ISSN : 2333-6455
Launched : 2013
Journal of Urology and Research
ISSN : 2379-951X
Launched : 2014
Journal of Family Medicine and Community Health
ISSN : 2379-0547
Launched : 2013
Annals of Pregnancy and Care
ISSN : 2578-336X
Launched : 2017
JSM Cell and Developmental Biology
ISSN : 2379-061X
Launched : 2013
Annals of Aquaculture and Research
ISSN : 2379-0881
Launched : 2014
Journal of Immunology and Clinical Research
ISSN : 2333-6714
Launched : 2013
Annals of Forensic Research and Analysis
ISSN : 2378-9476
Launched : 2014
JSM Biochemistry and Molecular Biology
ISSN : 2333-7109
Launched : 2013
Annals of Breast Cancer Research
ISSN : 2641-7685
Launched : 2016
Annals of Gerontology and Geriatric Research
ISSN : 2378-9409
Launched : 2014
Journal of Sleep Medicine and Disorders
ISSN : 2379-0822
Launched : 2014
JSM Burns and Trauma
ISSN : 2475-9406
Launched : 2016
Chemical Engineering and Process Techniques
ISSN : 2333-6633
Launched : 2013
Annals of Clinical Cytology and Pathology
ISSN : 2475-9430
Launched : 2014
JSM Allergy and Asthma
ISSN : 2573-1254
Launched : 2016
Journal of Neurological Disorders and Stroke
ISSN : 2334-2307
Launched : 2013
Annals of Sports Medicine and Research
ISSN : 2379-0571
Launched : 2014
JSM Sexual Medicine
ISSN : 2578-3718
Launched : 2016
Annals of Vascular Medicine and Research
ISSN : 2378-9344
Launched : 2014
JSM Biotechnology and Biomedical Engineering
ISSN : 2333-7117
Launched : 2013
Journal of Hematology and Transfusion
ISSN : 2333-6684
Launched : 2013
JSM Environmental Science and Ecology
ISSN : 2333-7141
Launched : 2013
Journal of Cardiology and Clinical Research
ISSN : 2333-6676
Launched : 2013
JSM Nanotechnology and Nanomedicine
ISSN : 2334-1815
Launched : 2013
Journal of Ear, Nose and Throat Disorders
ISSN : 2475-9473
Launched : 2016
JSM Ophthalmology
ISSN : 2333-6447
Launched : 2013
Journal of Pharmacology and Clinical Toxicology
ISSN : 2333-7079
Launched : 2013
Annals of Psychiatry and Mental Health
ISSN : 2374-0124
Launched : 2013
Medical Journal of Obstetrics and Gynecology
ISSN : 2333-6439
Launched : 2013
Annals of Pediatrics and Child Health
ISSN : 2373-9312
Launched : 2013
JSM Clinical Pharmaceutics
ISSN : 2379-9498
Launched : 2014
JSM Foot and Ankle
ISSN : 2475-9112
Launched : 2016
JSM Alzheimer's Disease and Related Dementia
ISSN : 2378-9565
Launched : 2014
Journal of Addiction Medicine and Therapy
ISSN : 2333-665X
Launched : 2013
Journal of Veterinary Medicine and Research
ISSN : 2378-931X
Launched : 2013
Annals of Public Health and Research
ISSN : 2378-9328
Launched : 2014
Annals of Orthopedics and Rheumatology
ISSN : 2373-9290
Launched : 2013
Journal of Clinical Nephrology and Research
ISSN : 2379-0652
Launched : 2014
Annals of Community Medicine and Practice
ISSN : 2475-9465
Launched : 2014
Annals of Biometrics and Biostatistics
ISSN : 2374-0116
Launched : 2013
JSM Clinical Case Reports
ISSN : 2373-9819
Launched : 2013
Journal of Cancer Biology and Research
ISSN : 2373-9436
Launched : 2013
Journal of Surgery and Transplantation Science
ISSN : 2379-0911
Launched : 2013
Journal of Dermatology and Clinical Research
ISSN : 2373-9371
Launched : 2013
JSM Gastroenterology and Hepatology
ISSN : 2373-9487
Launched : 2013
Annals of Nursing and Practice
ISSN : 2379-9501
Launched : 2014
JSM Dentistry
ISSN : 2333-7133
Launched : 2013
Author Information X