Journal of Cardiology and Clinical Research

What Can the Mitochondrial Disease Friedreich’s Ataxia Tell Us about the Aging Mitochondria?

Mini Review | Open Access | Volume 11 | Issue 2

  • 1. School of Medicine, University of New Mexico, USA
  • 2. Department of Internal Medicine, University of New Mexico, USA
+ Show More - Show Less
Corresponding Authors
Veena Raizada, Department of Internal Medicine, Cardiology Section, University of New Mexico, 2211 Lomas Blvd NE, Albuquerque, NM 87131, USA.

Friedrich’s Ataxia (FA) is a progressive neurodegenerative disorder commonly cited with a incidence of 1/50,000 live births. The disease is autosomal recessive and arises from a trinucleotide GAA repeat on chromosome 9. This repeat is located within the frataxin gene, which is located within the mitochondria and is commonly cited to be closely related to iron homeostasis within the mitochondria. Thus, FA is a neurodegenerative disease primarily arising from mitochondrial dysfunction. Clinically, FA presents in the first two decades of life, and is associated with significant morbidity and mortality. Clinical findings include truncal and limb ataxia, and absent deep tendon reflexes. Other findings include pes cavus, scoliosis, cardiomyopathy and dysarthria. FA results in several morphological, functional and biochemical abnormalities on the cellular and mitochondrial level. Moreover, several mitochondrial alterations have been linked to aging and age related diseases. The present mini-review will compare the common abnormalities found in the mitochondria due to normal aging and FA.


Friedreich ataxia, Aging, Mitochondria


Delahoussaye M, Raizada V. What Can the Mitochondrial Disease Friedreich’s Ataxia Tell Us about the Aging Mitochondria? J Cardiol Clin Res. 2023; 11(2): 1190.


Friedrich’s Ataxia is a neurodegenerative ataxia, afflicting anywhere between 1/15,000 to 1/200,000 of the population with geographical variation [1]. Patients with Friedrich’s Ataxia often present with ataxia, diabetes mellitus, and cardiac disease. The disease commonly presents in the first two decades of life with truncal and limb ataxia and absent deep tendon reflexes being among the most consistent clinical findings within 5 years of diagnosis. Other clinical findings include dysarthria (difficulty speaking), loss of joint position and vibratory sense, scoliosis, pes cavus, and cardiomyopathy. Indeed, most patients with FA will develop cardiomyopathy at some point in their life. Most patients are wheelchair bound within 15 years of diagnosis, or by age 25 [2].

The disease is caused by a mutation in the Frataxin gene which was first identified in 1996 [3].The genetic alterations occur due to a GAA tri-nucleotide repeat on chromosome 9 in the frataxin gene. Expansion of these repeats results in a misfolded and/or non-functioning frataxin protein, and decreased number of frataxin transcripts [4]. Normally, the protein contains less than 50 of these GAA repeats, whereas these expansions in Friedrichs ataxia may contain hundreds of trinucleotide repeats. The disease severity and age of onset is positively associated with the number of GAA repeats, with the age of onset occurring 2-3 years earlier for each additional 100 GAA repeats. Moreover, the number of GAA repeats is also correlated with a more rapidly progressing disease course [5].

Normal Mitochondrial Function and Morphology

Mitochondria are cellular organelles that are essential to eukaryotic life. Interestingly, mitochondria carry their own DNA, separate from the DNA which resides in the nucleus of the cell proper. This DNA is maternally inherited. They perform a variety of functions, including cellular respiration, fatty acid oxidation, ATP production, iron regulation and heme synthesis, among others [6]. Moreover, mitochondrial morphology has been studied extensively in regard to healthy mitochondria, as well as diseased and aging mitochondria. Healthy mitochondria have been shown to form networked arrays. This is thought to contribute to efficient energy production as well as aid in fission and fusion [7]. Individual mitochondria also have characteristic morphology, which can vary between which tissue the mitochondria reside in. Typically, they are represented as oblong structures, with an inner and outer membrane, with the inner membrane folding over on itself to form cristae [8]. It has been documented that diseased or stressed mitochondria can lose their characteristic morphology and network. These mitochondrial may decreased in size, or lose their shape or cristae [9] (Figure 1).

Normal Mitochondrial Function and Morphology.

Figure 1: Normal Mitochondrial Function and Morphology.

The Aging Mitochondria

Mitochondrial changes and dysfunction have long been linked to aging. Many changes to mitochondrial function and morphology have been shown to occur with aging over the past several decades. However, whether these changes are a byproduct of aging or whether they contribute to aging directly remains to be conclusively established.

In muscle tissue, mitochondrial ATP production and mitochondrial VO2 max both decreased by 5-8% per decade, when accounting for covariates. Moreover, mitochondrial protein expression of 12 proteins of interest declined by 8-10% per decade of life. Finally, and importantly, mtDNA content decreased with age and DNA oxidation increased with age [10]. What causes this oxidative DNA damage? Many have postulated that oxidative damage from free radicals was the primary driver of oxidative damage to mitochondria [11]. Several studies have been published which both support and refute this claim.

With ageing, mitochondria tend to exhibit decreased membrane potential and increased ROS production [12]. They also can develop and accumulate lipid particles, as seen in hepatic steatosis [13]. Non-heme iron has been shown to accumulate in mitochondria with age. This correlated with mtRNA damage and Ca++ handling capacity [14]. Non-heme iron has also been shown to accumulate in the cytosol and mitochondria in the brain cortex [15]. Finally, in C.elegens, mitochondria tend to fragment, have decreased volume, and a decrease in network capacity [16] (Figure 2).

Mitochondrial changes related to aging.

Figure 2: Mitochondrial changes related to aging.

Mitochondrial Pathophysiology in Friedrich’s Ataxia

Frataxin is a protein that is primarily found in the mitochondria, and has been located on normal human tissue in the muscle, heart cerebellum and spinal cord among other tissues [3]. Indeed, a review article from 2019 touched on the role frataxin deficiency in FA has been shown to contribute to deficiency in Fe-S clusters, iron overload in the mitochondria, and oxidative stress, and inflammation. Frataxin has many functions, including participating in the formation of essential Iron-sulfur clusters in the mitochondria [17,18]. These clusters have an important role in mitochondrial ECT function and respiration. It has been shown that a deficiency in any one of the proteins responsible for formation of the Fe-S clusters results in an accumulation of ‘free’ iron not related to heme or Fe-S synthesis [19]. Moreover, the dysfunction of frataxin and Fe-S clusters has been demonstrated to be linked to iron overload in the cytosol and mitochondria of cardiac myocytes in patients with FA. About 1-10% of cardiac myocytes will have iron granules, revealing a multifocal pattern of distribution [20].

In vitro frataxin knockdown cells were shown to result in mitochondrial dysfunction, altered mitochondrial membrane potential, reduced mitochondrial respiration and overall ATP production, and reduced cofactors essential for the formation of heme. In Frataxin knockdown cells, the mitochondria appeared fragmented and localized around the nucleus in juxtaposition to controls which were networked. Cells without frataxin exhibited hyperpolarized mitochondrial membrane potential which has been linked to ROS production [21]. As a consequence of increased iron accumulation and production on ROS, FA model mice have shown to lead to increased levels of neighboring lipid peroxidation in the mitochondria. Production of these lipoperoxidation products contributes to damage of cellular compartments and eventual cell death [22].

Cells without frataxin also had decreased cellular respiration, O2 utilization, and decreased ATP production. In addition, cells that were rescued with an iron storage protein in frataxin suppressed cells could reduce the accumulation of free iron, returning some normal mitochondrial function. Finally, the authors showed that frataxin knockdown resulted in higher rates of ferroptosis compared to controls [23,24].

In Mice with frataxin knock out, the mitochondria exhibited structural abnormalities such as decrease in number and with increased size and irregular cristae. These mitochondria also had lower rate of oxygen consumption [25] (Figure 3).

Mitochondria showing iron accumulation leading to ROS and  Superoxide Production.

Figure 3: Mitochondria showing iron accumulation leading to ROS and Superoxide Production.

Iron, Diabetes in FA

Many patients with FA go on to develop type 2 diabetes, with estimates reported between 10%-30% of patients [26]. A large multicenter study published in 2022 found an 8.7% incidence of DM in FA patients [27]. Research has shown that individuals with T2D have decreased levels of leukocyte frataxin compared to controls without T2D. This association was independent of confounding factors such as gender, albumin, hypertension and BMI. Notably, these patients with T2D were not patients with FA but still had a relative deficiency in frataxin [23]. These findings add to the growing body of evidence that mitochondrial dysfunction has a significant role in the development of insulin resistance and type 2 diabetes. It has been shown previously that acquired defects in mitochondrial proteins can directly cause Insulin resistance, the hallmark of T2D [29].

Frataxin knockout mice were shown to have decreased islet cell mass and islet cell number, leading to decreased insulin secretion capacity. Notably, the islet cell number was identical in both young FA knockout mice and young controls. However, the FA knockout mice showed reduced islet cell mass, suggesting the loss of mass was acquired as the mouse aged. Frataxin deficiency also leads to an increase in ROS and free radicals in pancreatic islet cells, predominately superoxide. The increase in ROS is thought to be related to increased free iron in the cell and mitochondria secondary to frataxin deficiency. Dysregulated iron has been linked to an increase in mitochondrial ROS [30].

Mitochondria, Cardiomyopathy in FA

Cardiomyopathy is one of the primary derangements seen in FA. It is seen in up to 1/3 of patients and is the single leading cause of death in FA [3]. Both lipofuscin and free iron aggregates have been found in the cardiomyocytes of FA patients, along with the typical fibrosis and hypertrophy expected from cardiomyopathy [31]. One study showed that Frataxin KO mice exhibited a relative cardiomyocyte cytosolic iron deficiency, along with mitochondrial iron overload. Moreover, they showed that iron supplementation could limit the extend of cardiomyopathy, presumably by rescuing cytosolic iron content. They also postulated that the relative Frataxin deficiency in certain organs led to alterations in systemic iron homeostasis [32]. However, there is debate as to if iron accumulation is a causative factor in organ dysfunction or a incidental byproduct. Although the toxic effects of frataxin loss have been documented on a cellular level, some studies have shown that frataxin deficiency without iron overload and sufficient to cause embryonic death. This is consistent with the model of human FA, in which some frataxin expression is preserved, at least for some time [2,33].


Friedrich’s Ataxia is a mitochondrial disease leading to significant morbidity and mortality in this afflicted. Research has elucidated several morphological, functional, and biochemical abnormalities seen in the mitochondria of patients with FA or models with an equivalent frataxin deficiency [17,18,25]. Moreover, the mitochondrion have become an area of interest and research in regards to the role they potentially play in aging. Indeed, both aging mitochondrion and those in FA have been shown to exhibit impaired iron homeostasis and accumulated of non-heme iron [14,31]. In FA, this accumulation is thought to be due to a relative deficiency in Frataxin, and occurs at a highly accelerated rate compared to non-diseased cells. In a normal aging cell, this accumulation occurs over many more decades and is thought to be due to cumulative effects of inflammation and ROS on mitochondrial proteins and mtDNA.

Moreover, OXPHOS and respiratory dysfunction is seen in both FA cells and in aging cells. Aging mitochondria in muscle cells shows a 5-8% decrease in ATP production and VO2max. Similarly, FA cells in vitro had a significant decrease in ATP production and O2 consumption. The decrease in the frataxin model was identified as being due to a defect in complex IV of the ECT. In aging cells, the decrease was postulated to be due to an accumulation of ROS, mtDNA damage, and a decrease in protein function and number [10,24].

Morphological changes occur in both FA, frataxin deficient models, and in normal aging. In FA models, mitochondria exhibited a decrease in number, size, and abnormalities in cristae structure [25]. Mitochondria in C.elegens exhibit fragmentation, decreased volume, and a decreased capacity to form mitochondrial networks.


Mitochondrial function is significantly altered in FA and FA models, and in normal aging. Several alterations are common to both, such as irregular iron homeostasis, decreased oxidative capacity, increased production of ROS, mtDNA damage, and morphological changes. Despite these abnormalities, it is unclear as to which abnormalities are a consequence of aging, or a direct driver of aging and dysfunction.

Authors Contributions

Michael Delahoussaye, School of Medicine, University of New Mexico.

Veena Raizada, Department of Internal Medicine, Cardiology Section, University of New Mexico, Albuquerque, NM 87106, United States.


1. Vankan P. Prevalence gradients of Friedreich’s Ataxia and R1b haplotype in Europe co-localize, suggesting a common Palaeolithic origin in the Franco-Cantabrian ice age refuge. J Neurochem. 2013; 126: 11-20.

2. Harding AE. Friedreich’s ataxia: a clinical and genetic study of 90 families with an analysis of early diagnostic criteria and intrafamilial clustering of clinical features. Brain. 1981; 104: 589-620.

3. Campuzano V, Montermini L, Lutz Y, Cova L, Hindelang C, Jiralerspong S, et al. Frataxin is reduced in Friedreich ataxia patients and is associated with mitochondrial membranes. Hum Mol Genet. 1997; 6: 1771-1780.

4. Bidichandani SI, Ashizawa T, Patel PI. The GAA triplet-repeat expansion in Friedreich ataxia interferes with transcription and may be associated with an unusual DNA structure. Am J Hum Genet. 1998; 62: 111-121

5. Reetz K, Dogan I, Costa AS, Dafotakis M, Fedosov K, Giunti P, et al. Biological and clinical characteristics of the European Friedreich’s Ataxia Consortium for Translational Studies (EFACTS) cohort: a cross-sectional analysis of baseline data. Lancet Neurol. 2015; 14: 174-182.

6. Nunnari J, Suomalainen A. Mitochondria: in sickness and in health. Cell. 2012; 148: 1145-1159.

7. De Giorgi F, Lartigue L, Ichas F. Electrical coupling and plasticity of the mitochondrial network. Cell Calcium. 2000; 28: 365-370.

8. Bereiter-Hahn J, Vöth M. Dynamics of mitochondria in living cells: shape changes, dislocations, fusion, and fission of mitochondria. Microsc Res Tech. 1994; 27: 198-219.

9. Gilkerson RW, Margineantu DH, Capaldi RA, Selker JM. Mitochondrial DNA depletion causes morphological changes in the mitochondrial reticulum of cultured human cells. FEBS Lett. 2000; 474: 1-4.

10. Short KR, Bigelow ML, Kahl J. Decline in skeletal muscle mitochondrial function with aging in humans. Proc Natl Acad Sci USA. 2005; 102: 5618-5623.

11. HARMAN D. Aging: a theory based on free radical and radiation chemistry. J Gerontol. 1956; 11: 298-300.

12. Passos JF, Saretzki G, Ahmed S, Nelson G, Richter T, Peters H, et al. Mitochondrial dysfunction accounts for the stochastic heterogeneity in telomere-dependent senescence. PLoS Biol. 2007; 5: e110.

13. Ogrodnik M, Miwa S, Tchkonia T, Tiniakos D, Wilson CL, Lahat A, et al. Cellular senescence drives age-dependent hepatic steatosis. Nat Commun. 2017; 8: 15691.

14. Seo AY, Xu J, Servais S, Hofer T, Marzetti E, Wohlgemuth, et al. Mitochondrial iron accumulation with age and functional consequences. Aging Cell. 2008; 7: 706-716.

15. Tatsuya Sato, Jason Solomon Shapiro, Hsiang-Chun Chang, Richard A Miller, Hossein Ardehali. Aging is associated with increased brain iron through cortex-derived hepcidin expression eLife. 2022; 11: e73456.

16. Regmi SG, Rolland SG, Conradt B. Age-dependent changes in mitochondrial morphology and volume are not predictors of lifespan. Aging (Albany NY). 2014; 6: 118-130.

17. Fox NG, Yu X, Feng X, Bailey HJ, Martelli A, Nabhan JF, et al. Structure of the human frataxin-bound iron-sulfur cluster assembly complex provides insight into its activation mechanism Nat Commun. 2019; 10: 2210

18. Martin B. Delatycki, Sanjay I. Bidichandani. Friedreich ataxiapathogenesis and implications for therapies. Neurobiol Dis. 2019; 132: 104606

19. Kispal G, Csere P, Prohl C, Lill R. The mitochondrial proteins Atm1p and Nfs1p are essential for biogenesis of cytosolic Fe/S proteins. The EMBO J. 1999; 18: 3981-3989.

20. Gonzalez-Cabo P, Palau F. Mitochondrial pathophysiology in Friedreich’s ataxia. J Neurochem. 2013; 126: 53-64.

21. Hüttemann M, Lee I, Pecinova A, Pecina P, Przyklenk K, Doan JW. Regulation of oxidative phosphorylation, the mitochondrial membrane potential, and their role in human disease J Bioenerg Biomembr. 2008; 40: 445-456

22. Abeti R, Parkinson MH, Hargreaves IP, Angelova PR, Sandi C, Pook MA, et al. ‘Mitochondrial energy imbalance and lipid peroxidation cause cell death in Friedreich’s ataxia’. Cell Death Dis. 2016; 7: e2237.

23. Du J, Zhou Y, Li Y, Xia J, Chen Y, Wang X, et al. Identification of Frataxin as a regulator of ferroptosis. Redox Biol. 2020; 32: 101483.

24. Bolinches-Amorós A, Mollá B, Pla-Martín D, Palau F, GonzálezCabo P. Mitochondrial dysfunction induced by frataxin deficiency is associated with cellular senescence and abnormal calcium metabolism. Front Cell Neurosci. 2014; 8: 124.

25. Turchi R, Tortolici F, Guidobaldi G, Lacovelli F, Falconi M, Rufini S, et al. Frataxin deficiency induces lipid accumulation and affects thermogenesis in brown adipose tissue [published correction appears in Cell Death Dis. Cell Death Dis. 2020; 11: 51.

26. Cnop M, Mulder H, Igoillo-Esteve M. Diabetes in Friedreich ataxia. J Neurochem. 2013; 126: 94-102.

27. Tamaroff J, DeDio A, Wade K, Wells M, Park C, Leavens K, et al. Friedreich’s Ataxia related Diabetes: Epidemiology and management practices. Diabetes Res Clin Pract. 2022; 186: 109828.

28. Du J, Zhou Y, Li Y, Xia J, Chen Y, Wang X, et al. Identification of Frataxin as a regulator of ferroptosis. Redox Biol. 2020; 32: 101483.

29. Zhang D, Liu ZX, Choi CS, Tian L, Kibbey R, Dong J, et al. Mitochondrial dysfunction due to long-chain Acyl-CoA dehydrogenase deficiency causes hepatic steatosis and hepatic insulin resistance. Proc Natl Acad Sci U S A. 2007; 104: 17075-17080.

30. Ristow M, Mulder H, Pomplun D, Schulz TJ, Müller-Schmehl K, Krause A, et al. Frataxin deficiency in pancreatic islets causes diabetes due to loss of beta cell mass. J Clin Invest. 2003; 112: 527-534.

31. Lamarche JB, Côté M, Lemieux B. The cardiomyopathy of Friedreich’s ataxia morphological observations in 3 cases. Can J Neurol Sci. 1980; 7: 389-396.

32. Whitnall M, Suryo Rahmanto Y, Huang ML, Saletta F, Lok HC, Gutiérrez L, et al. Identification of nonferritin mitochondrial iron deposits in a mouse model of Friedreich ataxia. Proc Natl Acad Sci U S A. 2012; 109: 20590-20595.

33. Cossée M, Puccio H, Gansmuller A, Koutnikova H, Dierich A, LeMeur M, et al. Inactivation of the Friedreich ataxia mouse gene leads to early embryonic lethality without iron accumulation. Hum Mol Genet. 2000; 9: 1219-1226.

Delahoussaye M, Raizada V. What Can the Mitochondrial Disease Friedreich’s Ataxia Tell Us about the Aging Mitochondria? J Cardiol Clin Res. 2023; 11(2): 1190.

Received : 15 Aug 2023
Accepted : 19 Sep 2023
Published : 21 Sep 2023
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
Clinical Research in Pulmonology
ISSN : 2333-6625
Launched : 2013
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
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